The DOI matches its Crossref record; 263 of the 281 references it cites were found in a registry or an index; 158 of the 267 sources its claims cite were checked for support.
NODDI in clinical research
Open accessAbstract
Diffusion MRI (dMRI) has proven to be a useful imaging approach for both clinical diagnosis and research investigating the microstructures of nervous tissues, and it has helped us to better understand the neurophysiological mechanisms of many diseases. Though diffusion tensor imaging (DTI) has long been the default tool to analyze dMRI data in clinical research, acquisition with stronger diffusion weightings beyond the DTI regimen is now possible with modern clinical scanners, potentially enabling even more detailed characterization of tissue microstructures. To take advantage of such data, neurite orientation dispersion and density imaging (NODDI) has been proposed as a way to relate the dMRI signal to tissue features via biophysically inspired modeling. The number of reports demonstrating the potential clinical utility of NODDI is rapidly increasing. At the same time, the pitfalls and limitations of NODDI, and general challenges in microstructure modeling, are becoming increasingly recognized by clinicians. dMRI microstructure modeling is a rapidly evolving field with great promise, where people from different scientific backgrounds, such as physics, medicine, biology, neuroscience, and statistics, are collaborating to build novel tools that contribute to improving human healthcare. Here, we review the applications of NODDI in clinical research and discuss future perspectives for investigations toward the implementation of dMRI microstructure imaging in clinical practice.
Overview
AI snapshot
Written from the paper’s full text.
TL;DR
NODDI is a three-compartment biophysical diffusion MRI model that estimates neurite density index (NDI), orientation dispersion index (ODI), and free water fraction, and this review surveys its clinical research applications across neurological and psychiatric diseases. It reports generally promising disease sensitivity and acceptable repeatability, but emphasizes unresolved model-specificity and validation limitations that keep NODDI short of routine clinical use.
Key findings
- NODDI uses NDI/intra-neurite fraction, ODI (0 for perfectly aligned straight fibers, 1 for completely isotropic), and free water fraction; it has 5 free parameters, one fewer than DTI, and imposes constraints including fixed parallel diffusivity 1.7 µm²/ms and a tortuosity model.
- Scan-rescan repeatability in brain is excellent for NDI and ODI, with intra-subject coefficients of variation mostly below 5%, comparable to DTI; free water fraction is less stable (10%–40% CoV). Field strength and scanner affect reproducibility.
- Across diseases (Alzheimer’s, Parkinson’s, MS, ALS, epilepsy, ischemia, TBI, NF1, iNPH, schizophrenia, tumors, spondylotic myelopathy), NODDI often detects abnormalities more widespread than FA, e.g., reduced NDI in WM/lesions and variable ODI; however, findings are mixed and mostly cross-sectional.
- NODDI is more specific than FA, and ODI correlates more strongly than FA with histological orientation dispersion, but specificity is only relative; the review concludes NODDI remains near the translational gap for clinical biomarker adoption.
Methods
- Narrative review of clinical research applications of NODDI, including human studies and some preclinical/animal evidence, organized by disease and by development/aging.
- No systematic search strategy, meta-analysis, or pooled quantitative synthesis is described in the text.
- Main analysis is thematic synthesis of reported NODDI findings, model rationale, repeatability/reproducibility evidence, and future directions.
Limitations
- The paper states that NODDI’s model assumptions remain debated: no consensus on compartment number; inter-compartmental exchange and non-Gaussian effects are neglected; fixed/constrained parameters can bias estimates; different constraints can change rankings; optimal fixed diffusivity may differ by age and tissue; parameter–pathology relationships are not one-to-one and pathologies coexist.
- The paper states that most clinical studies are cross-sectional, single-center, and limited in sample size, making general conclusions about individual patient care difficult; clinical adoption requires technical, biological/clinical, and cost-effectiveness validation.
- Evident from the text: this is a narrative review without a stated systematic search or meta-analysis, and many included findings are described as preliminary/proof-of-concept.
Model-written summary. Check it against the paper before relying on it.
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Verification
Claims the paper makes
158 of 267 cited sources checked · 109 supported · 2 flagged · accuracy not yet measured
At least one cited source doesn’t support this claim or points to a different paper, and none confirmed it — see the verdicts below.
In the paper
“A longitudinal follow-up of patients with orthopedic trauma revealed increased f fw and decreased NDI in WM compared with controls at 2 weeks post-injury”
§ NODDI in clinical research > 3.7. Traumatic brain injury
What the sources say
- Disputedcites Palacios et al., 2018 sourceExperimental — accuracy not yet measured
The Discussion identifies orthopedic trauma patients as the control group, not the group with these changes. It reports decreased NDI and increased free-water fraction (FISO) in patients with mTBI versus trauma controls at the early, 2-week time point. The supplied passages do not give page numbers. (LLM, conf=0.90)
Checked by a reasoning model — may be wrong.
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Disputed
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Care is needed in the interpretation of results provided by these biophysical models, because to achieve and prove specificity is extremely challenging (for recent reviews, see (Jelescu and Budde, 2017;Novikov et al., 2018a); and Jelescu et al. in this special issue).”
§ NODDI in clinical research > 2. Rationale for using NODDI in clinical research
What the sources say
- Supportedcites Jelescu and Budde, 2017 source
Section 2.3 cautions that even a strong correlation with microscopy does not prove parameter specificity. The Summary adds that diffusion MRI is an indirect measure of microstructure and that some model parameters are particularly difficult to validate independently. Together, these passages support the citing sentence’s caution about achieving and demonstrating specificity. (LLM, conf=0.91)
- Not matchedcites Novikov et al., 2018a
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes? Checkable: unclear✓ Load-bearing: passes✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“NDI of the parieto-occipital WM was also correlated with visuospatial and visuoperceptual cognitive performance, a marker of parietal cortex function.”
§ NODDI in clinical research > 3.1. Alzheimer's disease
What the sources say
- Supportedcites Slattery et al., 2017 source
The Results section reports significant positive correlations in patients between NDI in white-matter projections from both parieto-occipital lobes and visuospatial and visuoperceptual task performance. The Discussion identifies that performance as a marker of parietal cortex function, and the paper identifies the patient group as having young-onset Alzheimer’s disease. (LLM, conf=0.94)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“However, as with DTI, care should be taken when comparing data from different scanners: field strength has significant effects on NODDI parameters (Chung et al., 2016;De Santis et al., 2019), and interscanner reproducibility has been shown to be lower than intra-scanner reproducibility, even at the same field strength (3 T) (Andica et al., 2019b).”
§ NODDI in clinical research > 2.3. Is NODDI reliable?
What the sources say
- Supportedcites Chung et al., 2016 source
The Discussion states that magnetic field strength has a significant effect on estimated NODDI parameters. The Conclusion reports significant changes in intracellular volume fraction and orientation distribution index in specific white and grey matter regions and advises care when interpreting data acquired at different field strengths. (LLM, conf=0.94)
- Partly supportedcites De Santis et al., 2019 sourceExperimental — accuracy not yet measured
The Statistical analysis section compares 3 T and 7 T protocols for the NODDI measures. Table 3 (DISCUSSION; page unavailable) reports a significant protocol effect for FR NODDI (p < 0.05), but not for ODI. The claim is therefore supported for one NODDI parameter, not NODDI parameters generally. (LLM, conf=0.88)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Several studies have reported non-monotonic behavior of dMRI metrics in relation to amyloid deposition in both GM (Montal et al., 2018) and WM (Dong et al., 2020;Wolf et al., 2015) in human Alzheimer's disease, as well as in a rat model of Alzheimer's disease (Fick et al., 2017).”
§ NODDI in clinical research > 3.1. Alzheimer's disease
What the sources say
- Not checked — no full text of the sourcecites Montal et al., 2018 source
- Supportedcites Dong et al., 2020 source
Dong et al.’s Results (ROI Analysis: Group comparisons; page not provided) report nonmonotonic white-matter diffusion metric changes across groups with increasing amyloid burden. The Abstract likewise reports a nonmonotonic trend in human participants. This citation supports the white-matter portion of the sentence; the gray-matter and rat-model portions are attributed to other sources. (LLM, conf=0.94)
- Not checked — no full text of the sourcecites Wolf et al., 2015 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesEvery source the paper cites for this claim was checked and supports it.
In the paper
“ODI has shown a stronger correlation than has FA with orientation dispersion measured by histology (Grussu et al., 2017;Schilling et al., 2018), indicating that NODDI has the ability, at least partly, to disentangle the effect of orientation dispersion.”
§ NODDI in clinical research > 2.2. Is NODDI specific?
What the sources say
- Supportedcites Grussu et al., 2017 source
The Results (Statistical analysis; page not supplied) report a strong correlation between ODI and histological orientation dispersion (CV). In the control samples, regression models show a stronger association with CV for ODI than for FA; the paper also describes ODI–CV as the strongest and most consistent association across controls and multiple sclerosis cases. (LLM, conf=0.90)
- Supportedcites Schilling et al., 2018 source
In Results §3.1 (Fig. 7E–F), the paper reports a moderate negative correlation between DTI FA and histological ODI, while describing NODDI’s correlation with histological ODI as much stronger overall. The passage supports the comparison in the citing sentence; the paper notes that NODDI overestimated ODI in its ex vivo experiments. (LLM, conf=0.86)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Similarly, in another mouse model of Alzheimer's disease, greater NDI and ODI than controls were observed in WM and hippocampus (Colon-Perez et al., 2019).”
§ NODDI in clinical research > 3.1. Alzheimer's disease
What the sources say
- Supportedcites Colon-Perez et al., 2019 source
The Results report higher intracellular volume fraction (ICVF), the paper’s neurite-density measure, in the cerebral peduncle (white matter) and hippocampus of TgCRND8 mice, and higher ODI in white-matter regions and the hippocampus. The Discussion explicitly describes increases in both measures relative to non-transgenic controls. The supplied passages do not give page numbers. (LLM, conf=0.93)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Scan-rescan studies have reported excellent repeatability of NODDI in the brain, with the intra-subject coefficients of variation (CoV) for NDI and ODI mostly below 5% (Andica et al., 2019b;Chang et al., 2015;Chung et al., 2016;Granberg et al., 2017;Huber et al., 2019;Tariq et al., 2012), which is comparable with that of DTI, although (Chung et al., 2016) have reported a greater CoV than for FA in”
§ NODDI in clinical research > 2.3. Is NODDI reliable?
What the sources say
- Not matchedcites Andica et al., 2019b
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Supportedcites Chang et al., 2015 source
Results §3.5 reports that test–retest CoVs for ODI and NDI were below 5% in every examined white matter group. Discussion §4.3 calls the reproducibility excellent and notes that repeat scans were limited to adults in their 20s. (LLM, conf=0.93)
- Partly supportedcites Chung et al., 2016 sourceExperimental — accuracy not yet measured
The Methods and Results describe repeated acquisitions within a session in healthy subjects and report within-subject CVs for NODDI measures. The Discussion gives a range of 0.6%–7.3% (excluding νiso), but does not establish that NDI and ODI values were mostly below 5%; this was within-session reproducibility, not a separate-session scan–rescan test. (LLM, conf=0.84)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Not matched
Every source the paper cites for this claim was checked and supports it.
In the paper
“(Lampinen et al., 2019) clarified the risk of biases introduced by fixing parameters, where different constraints led to different rankings of neurite density among brain regions.”
§ NODDI in clinical research > 2.2. Is NODDI specific?
What the sources say
- Supportedcites Lampinen et al., 2019 source
The Results section, under “Brain region rankings by the ‘stick’ fractions of constrained biophysical models,” reports that six constraint sets produced significantly different regional rankings (p = 0.025). The paper treats these model-derived ‘stick’ fractions as indices of neurite density, which is the sense in which the citing sentence is supported. (LLM, conf=0.91)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In a longitudinal follow-up, ODI in the posterior limb of the internal capsule at the first hospital visit predicted upper extremity motor function at 5-week follow-up (Hodgson et al., 2019).”
§ NODDI in clinical research > 3.6. Ischemia
What the sources say
- Supportedcites Hodgson et al., 2019 source
The Conclusions report that baseline ODI asymmetry in the posterior limb of the internal capsule (PLIC) predicted upper-extremity motor outcomes approximately five weeks after stroke. The Abstract specifies that the baseline MRI was obtained 3–12 days after stroke and that the follow-up outcome was an upper-extremity Fugl-Meyer score. The measured predictor was ODI-based asymmetry between the two sides of the PLIC, rather than ODI alone. (LLM, conf=0.91)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Within the CST distal to the lesion, increased ODI has been observed in the subacute phase and this increase persisted in the chronic phase (Mastropietro et al., 2019).”
§ NODDI in clinical research > 3.6. Ischemia
What the sources say
- Supportedcites Mastropietro et al., 2019 source
The Discussion reports significantly higher ODI in the ipsilesional PLIC and CP regions of the CST in the subacute phase. The chronic-phase Results report persistently higher ODI in both regions, including the more distal CP (p = 0.014). (LLM, conf=0.94)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“indicating that NODDI's assumptions of fixed diffusivity and tortuosity constraints are most likely broken.”
§ NODDI in clinical research > 3.6. Ischemia
What the sources say
- Partly supportedcites Ackerman and Neil, 2010 sourceExperimental — accuracy not yet measured
In “Mechanism for the Water ADC Decrease That Accompanies Brain Injury” (page unavailable), the paper challenges an older model’s assumption that compartmental diffusivities remain unchanged after injury and suggests intracellular diffusivity decreases. It does not discuss NODDI or establish that NODDI’s tortuosity constraint is broken in acute cerebral ischemia. (LLM, conf=0.83)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“preclinical studies in acute cerebral ischemia using compartment-specific tracers have shown a profound decrease of diffusivities in both intra-and extra-cellular spaces (Ackerman and Neil, 2010)”
§ NODDI in clinical research > 3.6. Ischemia
What the sources say
- Supportedcites Ackerman and Neil, 2010 source
The “Changes in ADC Following Brain Injury” section reports that, after global ischemia, the compartment-specific FDG-6-P tracer’s ADC fell from 0.16 to 0.10 μm²/ms intracellularly and from 0.14 to 0.09 μm²/ms extracellularly. These substantial decreases support the claim about tracer-measured diffusivity in both spaces; the supplied passage has no page number. (LLM, conf=0.92)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“They also found that patients with secondary progressive MS showed more widespread NDI reduction than those with relapsing-remitting MS, suggesting the potential utility of NODDI for predicting transition from relapsing-remitting MS to secondary progressive MS.”
§ NODDI in clinical research > 3.3. Multiple sclerosis
What the sources say
- Supportedcites Spanò et al., 2018 source
The Discussion reports a widespread decrease in NDI in patients with secondary progressive MS and says neurite abnormalities were less extensive in those with relapsing-remitting MS. The Abstract Results likewise describe more widespread abnormalities in the secondary progressive group. Page numbers were not available in our copy. (LLM, conf=0.94)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The study of postmortem spinal cord by (Grussu et al., 2017) also revealed that NDI should be interpreted in relation to both neurite density and myelin density.”
§ NODDI in clinical research > 3.3. Multiple sclerosis
What the sources say
- Supportedcites Grussu et al., 2017 source
The Discussion (Statistical analysis) says NDI is sensitive to local axon and dendrite density but is also strongly influenced by myelination, limiting its interpretation without myelin mapping. The Discussion (Limitations) likewise cautions that myelin can affect NDI. This supports interpreting NDI in relation to both neurite and myelin density. (LLM, conf=0.94)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“and that reduced ODI within the precentral gyrus was correlated with disease duration, presumably representing reduced dendritic density and branching.”
§ NODDI in clinical research > 3.4. Amyotrophic lateral sclerosis
What the sources say
- Supportedcites Broad et al., 2019 source
The Results section ('Correlation of NODDI parameters with disease severity'; page unavailable) reports that ODI correlated with disease duration predominantly in the right precentral gyrus, with a smaller region in the left. The Discussion (page unavailable) interprets reduced ODI in this region as compatible with loss of dendritic density and reduced dendritic branching. (LLM, conf=0.94)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Recently, (Taoka et al., 2020) applied NODDI in 11 cases of tuberous sclerosis and confirmed reduced NDI in tubers.”
§ NODDI in clinical research > 3.5. Epilepsy
What the sources say
- Supportedcites Taoka et al., 2020 source
The Abstract reports NODDI imaging in 11 tuberous sclerosis cases. The Discussion identifies Ficv as a measure of neurite density and reports decreased Ficv in quantitative measurements of tubers. Page numbers are not provided in our copy. (LLM, conf=0.91)
Strength:plain· not yet calibratedn = 11Tests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“In WM, along-tract analysis of the nigro-striatal pathway (Andica et al., 2018) demonstrated reduced NDI in the tract portion proximal to the striatum, which is consistent with histological evidence of retrograde axonal degeneration ('dying back') (Tagliaferro and Burke, 2016).”
§ NODDI in clinical research > 3.2. Parkinson's disease
What the sources say
- Not checked — no full text of the sourcecites Andica et al., 2018 source
- Supportedcites Tagliaferro and Burke, 2016 source
The cited paper supports the sentence’s interpretation, not the NDI finding, which the sentence attributes to Andica et al. In “Evidence from postmortem and imaging studies in humans” (page unavailable), it reports postmortem evidence of early striatal axon-terminal involvement and describes findings suggesting degeneration begins in distal axons and proceeds retrogradely. The paper presents this as evidence consistent with ‘dying back,’ rather than definitive proof of that pattern in the nigrostriatal tract. (LLM, conf=0.90)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesThe cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Using NODDI, (Broad et al., 2019) found reduced NDI along the corticospinal tract (CST) and the transcallosal fiber between the primary motor cortices, which is consistent with histological studies reporting axonal degeneration within these regions (Brownell et al., 1970;Swash et al., 2020).”
§ NODDI in clinical research > 3.4. Amyotrophic lateral sclerosis
What the sources say
- Supportedcites Broad et al., 2019 source
The Results section (‘Neurite orientation dispersion and density imaging’) reports reduced NDI in the ALS group along a large continuous region of the corticospinal tract and in the transcallosal connection fibres between the primary motor cortices. This directly supports the finding attributed to Broad et al. (LLM, conf=0.95)
- Supportedcites Brownell et al., 1970 source
Brownell et al. are cited for the histological finding, not the NODDI result. The passage on corticospinal degeneration reports a band of degeneration in the corpus callosum in case 18, presumed to affect fibres connecting the left and right Rolandic areas; it also traces degeneration along the pyramidal tract. The callosal observation is limited to that case. (LLM, conf=0.90)
- Partly supportedcites Swash et al., 2020 sourceExperimental — accuracy not yet measured
Swash et al. are cited for the histological consistency of the finding, not for Broad et al.’s NODDI result. The Neuropathology section reports pathological evidence of corticospinal-tract axonal degeneration, while the Imaging section says interhemispheric motor fibres are involved in ALS. Our copy does not clearly establish histological axonal degeneration specifically in those transcallosal fibres, and it does not report reduced NDI. (LLM, conf=0.82)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Using a model almost identical to NODDI, (Surova et al., 2016) observed only small differences between patients with Parkinson's disease and healthy controls.”
§ NODDI in clinical research > 3.2. Parkinson's disease
What the sources say
- Supportedcites Surova et al., 2016 source
The Methods describe the study’s neurite density imaging (NDI) analysis as a simplification of the NODDI model. The Results report small differences in NDI measures between Parkinson’s disease patients and healthy controls, with no significant age- and gender-adjusted differences in the examined deep grey-matter regions. The claim accurately summarizes those model-based findings. (LLM, conf=0.90)
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Using NODDI parameters from tractograms as weights for a brain network in a connectomics study, (Lemkaddem et al., 2014) found different patterns of network alterations between left and right TLE.”
§ NODDI in clinical research > 3.5. Epilepsy
What the sources say
- Supportedcites Lemkaddem et al., 2014 source
The Introduction says the study averaged the NODDI parameters ICVF and ODI along tracts to construct structural connectivity matrices for graph analysis. The Discussion section “Different structural connectivity alterations in RTLE and LTLE” explicitly reports different patterns of changes in right versus left TLE. Page numbers were not available in our copy. (LLM, conf=0.93)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Increased NDI and ODI and decreased f fw have been reported in acute infarction lesions (Adluru et al., 2014;Z. Wang et al., 2019b).”
§ NODDI in clinical research > 3.6. Ischemia
What the sources say
- Partly supportedcites Adluru et al., 2014 sourceExperimental — accuracy not yet measured
The Results report higher neurite density (NDI/ND) and ODI and a lower CSF fraction in stroke lesions than in contralesional regions. Methods §II.B says the two patients were scanned 7 and 9 days after stroke, consistent with an acute setting, but our copy does not identify their lesions specifically as infarctions. (LLM, conf=0.82)
- Not matchedcites Z. Wang et al., 2019b
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Furthermore, (Broad et al., 2019) found that NDI was reduced to a greater spatial extent in patients with both limb and bulbar involvement compared with those with limb involvement alone.”
§ NODDI in clinical research > 3.4. Amyotrophic lateral sclerosis
What the sources say
- Supportedcites Broad et al., 2019 source
The Results (Subgroup analysis using the NODDI parameters) report significantly reduced NDI in the right corona radiata and subcortical white matter in patients with both bulbar and limb involvement compared with those with limb-only involvement. The Discussion describes this as more extensive microstructural damage in the group with more widespread clinical involvement. (LLM, conf=0.88)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Patients with neurocognitive and psychiatric symptoms have a smaller NDI in the cerebral WM than those without neurocognitive and psychiatric symptoms (Andica et al., 2020).”
§ NODDI in clinical research > 3.2. Parkinson's disease
What the sources say
- Supportedcites Andica et al., 2020 source
The Results (TBSS analysis; page unavailable) report significantly lower intracellular volume fraction (ICVF) in cerebral white matter among Parkinson’s patients with neurocognitive and psychiatric symptoms than among those without. The Discussion identifies ICVF as a measure of neurite density, matching the claim’s NDI terminology. (LLM, conf=0.93)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In GM, (Spanò et al., 2018) observed a correlation between clinical disability and NODDI parameters.”
§ NODDI in clinical research > 3.3. Multiple sclerosis
What the sources say
- Supportedcites Spanò et al., 2018 source
The Results (ODI correlations; page not provided) report significant associations between clinical disability scores and the NODDI measure ODI in several gray-matter regions, including the cingulate gyrus, caudate nucleus, and thalamus. The Discussion also states that gray-matter abnormalities correlate with patients’ clinical disability. (LLM, conf=0.94)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In children with cerebral palsy caused by perinatal stroke, NDI and ODI in lesioned CST were both decreased compared with in contralateral CST”
§ NODDI in clinical research > 3.6. Ischemia
What the sources say
- Supportedcites Nemanich et al., 2019 source
The Results (NODDI metrics; page unavailable) report significantly lower intracellular volume fraction (ICVF, the paper’s neurite-density measure) and ODI in the lesioned than the nonlesioned CST. The paper frames these findings in relation to perinatal stroke, although its sample also included one participant with periventricular leukomalacia. (LLM, conf=0.90)
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Studies in athletes with repetitive head impact found increased NDI, ODI, and f fw in both GM and WM compared with in non-athletes and non-contact athletes (Caron et al., 2020;Mayer et al., 2017).”
§ NODDI in clinical research > 3.7. Traumatic brain injury
What the sources say
- Partly supportedcites Caron et al., 2020 sourceExperimental — accuracy not yet measured
The paper’s opening summary says it mapped NODDI measures in cortical and subcortical structures and white-matter tracts, and found athletes to have higher microstructural measures than non-athlete controls. The passages do not establish that NDI, ODI, and f_fw were each increased in both gray and white matter specifically in the head-impact group, or that this group had higher values than non-contact athletes. (LLM, conf=0.75)
- Partly supportedcites Mayer et al., 2017 sourceExperimental — accuracy not yet measured
The Results (dMRI results; page unavailable) report increased ODI and intracellular water fraction (Vic) in some gray- and white-matter regions of mixed-martial artists, and increased free-water fraction (Viso) in some regions. But Viso was reduced in other regions, so the findings do not establish a uniform increase in all three measures across both tissue types. The Methods (Participants; page unavailable) describe one physically active healthy-control group with no regular contact-sport history, not separate non-athlete and non-contact-athlete comparison groups. (LLM, conf=0.86)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Using NODDI in combination with multi-exponential T2 relaxometry, (Billiet et al., 2014) showed decreased NDI and prolonged T2 in the cellular water compartment (encompassing both intra-and extra-cellular water) compared with in normal-appearing WM.”
§ NODDI in clinical research > 3.8. Neurofibromatosis type 1
What the sources say
- Supportedcites Billiet et al., 2014 source
The Discussion reports decreased NDI and increased T2 relaxation of intra- and extracellular water in UBOs compared with contralateral normal-appearing white matter (cNAWM). The Introduction identifies that T2 component as combined intra- and extracellular water. (LLM, conf=0.94)
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Every source the paper cites for this claim was checked and supports it.
In the paper
“Moreover, smaller NDI within the cingulum was associated with greater genetic risk for schizophrenia (Drakesmith et al., 2019).”
§ NODDI in clinical research > 3.10. Schizophrenia
What the sources say
- Supportedcites Drakesmith et al., 2019 source
The Results (White-matter microstructure; page not provided) report that intracellular volume fraction (ICVF) in the left cingulum decreases as the schizophrenia penetrance score increases. The Methods identify ICVF as a NODDI microstructural measure, and the Discussion interprets its reduction as reflecting lower axon density. The association was specifically observed in the left cingulum of people carrying risk-associated copy number variants. (LLM, conf=0.88)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“with greater effects observed among those imaged after a longer period of time since their last concussion (Churchill et al., 2017).”
§ NODDI in clinical research > 3.7. Traumatic brain injury
What the sources say
- Supportedcites Churchill et al., 2017 source
The Abstract states that NODDI-related effects were greater among athletes imaged longer after their last concussion. The Multivariate Analysis of Clinical History specifies the direction: longer intervals were associated with higher intracellular volume fraction (a neurite-density measure) and lower ODI. (LLM, conf=0.93)
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The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“suggesting that NODDI is sensitive to the damage caused by chronic ischemia (Hara et al., 2019(Hara et al., , 2018) ) (Fig. 6).”
§ NODDI in clinical research > 3.6. Ischemia
What the sources say
- Not checked — no full text of the sourcecites Hara et al., 2019 source
- Supportedcites Hara et al., 2018 source
The Conclusions (page not specified) state that NODDI revealed microstructural ischemic damage in normal-appearing brain tissue in adults with moyamoya disease. The Discussion also links the measured microstructural changes to chronic ischemia. (LLM, conf=0.93)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesEvery source the paper cites for this claim was checked and supports it.
In the paper
“A smaller NDI in WM was also found in patients with first-episode psychosis (Rae et al., 2017).”
§ NODDI in clinical research > 3.10. Schizophrenia
What the sources say
- Supportedcites Rae et al., 2017 source
The Conclusions state that neurite density is reduced across white matter tracts in first-episode psychosis. The NODDI methods passage identifies the intracellular volume fraction as an index of neurite density, supporting the claim about smaller NDI in white matter. (LLM, conf=0.94)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“and decreased NDI and f fw over time from 2 weeks to 6 months (Palacios et al., 2018).”
§ NODDI in clinical research > 3.7. Traumatic brain injury
What the sources say
- Partly supportedcites Palacios et al., 2018 sourceExperimental — accuracy not yet measured
The ‘Longitudinal analysis of mTBI patients at 2 weeks vs 6 months’ section reports decreases in NDI and FISO over that interval, but those results are for patients with mild traumatic brain injury. The Participants section identifies orthopedic trauma patients as controls; the paper does not report the claimed longitudinal decreases for them. Page numbers are unavailable in our copy. (LLM, conf=0.88)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Decreased NDI and ODI and increased f fw were associated with more severe ischemic burden and cognitive impairments (Hara et al., 2019(Hara et al., , 2018)).”
§ NODDI in clinical research > 3.6. Ischemia
What the sources say
- Not checked — no full text of the sourcecites Hara et al., 2019 source
- Partly supportedcites Hara et al., 2018 sourceExperimental — accuracy not yet measured
The Conclusions and figure captions (page not given) report lower intracellular volume fraction (Vic, corresponding to NDI) and orientation dispersion (OD, corresponding to ODI) in adults with moyamoya disease, and correlations of these measures with neuropsychological performance. The Discussion links those changes to chronic ischemia, but our copy does not report increased f_fw or show that all three measures track greater ischemic burden. It also notes that some cognitive correlations weakened when patients and controls were analyzed separately. (LLM, conf=0.86)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesThe cited sources support only part of this claim — read each source’s verdict below.
In the paper
“and greater NDI was associated with greater grip strength (Nemanich et al., 2019).”
§ NODDI in clinical research > 3.6. Ischemia
What the sources say
- Partly supportedcites Nemanich et al., 2019 sourceExperimental — accuracy not yet measured
The Results section (Hand function and relationship to diffusion metrics; page unavailable) reports that greater grip strength correlated with asymmetry indices for ICVF, a NODDI density metric. It does not establish that greater NDI itself was associated with greater grip strength. The Participants section (page unavailable) also includes children with periventricular leukomalacia, so the finding is not specific to cerebral palsy caused by perinatal stroke. (LLM, conf=0.86)
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The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“indicating the effect of orientation prevails and hides the putative effect of axonal degeneration resulting in greater FA (Kamiya et al., 2017).”
§ NODDI in clinical research > 3.9. Idiopathic normal pressure hydrocephalus
What the sources say
- Partly supportedcites Kamiya et al., 2017 sourceExperimental — accuracy not yet measured
The Introduction hypothesizes that increased FA in the corticospinal tract reflects an increase from axon stretching mixed with a decrease from neurodegeneration. The Results (Human data) find increased orientational coherence and lower axon density in patients, but FA was only nonsignificantly higher. The claim overstates the evidence by saying the orientation effect definitively prevails and hides degeneration. (LLM, conf=0.86)
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The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Although there is no established imaging tool capable of detecting the neuronal damage in TBI (Eierud et al., 2014)”
§ NODDI in clinical research > 3.7. Traumatic brain injury
What the sources say
- Partly supportedcites Eierud et al., 2014 sourceExperimental — accuracy not yet measured
The Discussion says neuroimaging lacks the patient-level sensitivity and specificity to diagnose mild TBI, and the Introduction describes microscopic injury as difficult to detect in an individual. That supports the absence of an established diagnostic imaging tool for mild TBI, but not the broader claim that no imaging tool can detect neuronal damage in TBI generally; the Results describe CT detection of some trauma-related abnormalities. (LLM, conf=0.85)
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Every source the paper cites for this claim was checked and supports it.
In the paper
“The work of Nemanich et al. (2019) also showed that individuals with greater asymmetry of CST dMRI metrics experienced greater improvements following neuromodulatory/motor training intervention.”
§ NODDI in clinical research > 3.6. Ischemia
What the sources say
- Supportedcites Nemanich et al., 2019 source
The Results section (‘Hand function and relationship to diffusion metrics’) reports that greater improvement in AHA after the intervention was strongly correlated with asymmetry indices for several CST diffusion metrics. The Discussion (‘Relationship to hand function and response to intervention’) explicitly says participants with greater CST asymmetry showed greater AHA improvement. The Methods (‘Intervention’) identifies the treatment as motor training paired with real or sham tDCS. (LLM, conf=0.94)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In GM, decreased ODI in the neocortex with increasing age has been reported (Nazeri et al., 2015)”
§ NODDI in clinical research > 4.1. Normal development and aging: late childhood to old age
What the sources say
- Supportedcites Nazeri et al., 2015 source
The ‘Aging pattern of GM microstructure’ section reports a widespread decrease in neocortical ODI with advancing age in 45 healthy adults aged 21–84. Its cortical ROI analysis also found significant declines in 27 of 48 regions. (LLM, conf=0.95)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“which is in line with histology showing age-related decreases of dendritic complexity and density (Dickstein et al., 2007).”
§ NODDI in clinical research > 4.1. Normal development and aging: late childhood to old age
What the sources say
- Supportedcites Dickstein et al., 2007 source
The Introduction describes dendritic and spine loss or regression during normal aging. The section “Dendrite and dendritic spine changes during aging” reports regression of cortical dendritic arbors and reduced spine density in aged animals, supporting the histological comparison. The citation does not attribute the cortical ODI measurement itself to this paper. (LLM, conf=0.91)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In contrast, ODI in WM remains almost stable during the first two decades of life (Genc et al., 2017;Jelescu et al., 2015;Lynch et al., 2020;Mah et al., 2017).”
§ NODDI in clinical research > 4.2. Normal development and aging: perinatal to childhood
What the sources say
- Not checked — no full text of the sourcecites Genc et al., 2017 source
- Partly supportedcites Jelescu et al., 2015 sourceExperimental — accuracy not yet measured
The Results (§4.1) state that NODDI showed no trend in orientation dispersion with age across the three white-matter regions studied. However, the subjects were aged only 1 day to 2 years and 9 months (§3.1.1), so this paper does not establish stability throughout the first two decades of life. (LLM, conf=0.88)
- Supportedcites Lynch et al., 2020 source
The Discussion reports that ODI was not significantly associated with age in the majority of white matter tracts studied from infancy through adolescence. The Results (‘Mean ODI changes with age’) note weak age-related correlations in three tracts, consistent with the claim’s ‘almost stable’ qualification. (LLM, conf=0.88)
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesEvery source the paper cites for this claim was checked and supports it.
In the paper
“In an unusually large data set, (Cox et al., 2016) confirmed NDI decrease from middle to old age.”
§ NODDI in clinical research > 4.1. Normal development and aging: late childhood to old age
What the sources say
- Supportedcites Cox et al., 2016 source
The Methods identify ICVF as a measure of neurite density, and the Discussion reports decreasing ICVF from middle to older age. The study’s 3,513 UK Biobank participants support the description of an unusually large data set. The finding is a cross-sectional age association, not a measured decline within individuals. (LLM, conf=0.92)
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The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In subjects with harmful alcohol use, ODI in the ventral striatum was positively correlated with binge score.”
§ NODDI in clinical research > 3.14. Effects of drugs and substance abuse
What the sources say
- Partly supportedcites Morris et al., 2018 sourceExperimental — accuracy not yet measured
The Results (Neurite orientation dispersion and density; page not available) report a positive correlation between ventral striatal ODI and binge score in binge drinkers. The Participants section identifies the studied group specifically as young adult binge drinkers, not subjects with harmful alcohol use generally; the claim broadens the population. (LLM, conf=0.84)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Discrepancy between clinical severity and degree of spinal cord compression is often encountered (Baron and Young, 2007;Nouri et al., 2016).”
§ NODDI in clinical research > 3.12. Spondylotic myelopathy
What the sources say
- Not checked — no full text of the sourcecites Baron and Young, 2007 source
- Partly supportedcites Nouri et al., 2016 sourceExperimental — accuracy not yet measured
The review’s discussion of spinal cord compression says it can occur in approximately 5% of asymptomatic patients, showing that compression and clinical symptoms do not always align. The Perspectives section also notes controversy about the association between cervical myelopathy and MRI findings. Neither passage establishes that discrepancies between clinical severity and the degree of compression are often encountered in patients with myelopathy. (LLM, conf=0.79)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesThe cited sources support only part of this claim — read each source’s verdict below.
In the paper
“(Cox et al., 2016) also found that dMRI parameters, including those of NODDI, become increasingly correlated across WM tracts in older age”
§ NODDI in clinical research > 4.1. Normal development and aging: late childhood to old age
What the sources say
- Partly supportedcites Cox et al., 2016 sourceExperimental — accuracy not yet measured
The Results section (‘Age de-differentiation of white matter microstructure’; page not provided) reports stronger covariation across tracts at older ages for several dMRI measures, including the NODDI measures ICVF and ISOVF. It explicitly excludes the NODDI measure OD, for which there was no appreciable age-related increase. The claim is therefore too broad if read to include NODDI parameters generally. (LLM, conf=0.88)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“ODI generally showed a nonlinear increase until around 60 years, followed by a decrease.”
§ NODDI in clinical research > 4.1. Normal development and aging: late childhood to old age
What the sources say
- Supportedcites Cox et al., 2016 source
The Discussion states that OD generally increased nonlinearly until around age 60, then decreased, with variation across tracts. This directly supports the attributed trajectory; the paper calls the measure OD rather than ODI. (LLM, conf=0.95)
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The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The performance of NODDI for tumor grading is comparable with that of mean kurtosis (Figini et al., 2018;Maximov et al., 2017)”
§ NODDI in clinical research > 3.11. Brain tumors
What the sources say
- Partly supportedcites Figini et al., 2018 sourceExperimental — accuracy not yet measured
The section “Correlation of Diffusion MRI Metrics with Glioma Grade, Histotype, and Cell Proliferation Index” (p. 5) reports that both NODDI and diffusion-kurtosis metrics distinguished grade IV from grade II and III gliomas, while neither distinguished grade II from grade III. This supports a broad similarity, but the paper does not directly compare NODDI’s tumor-grading performance with that of mean kurtosis specifically. (LLM, conf=0.82)
- Not checked — no full text of the sourcecites Maximov et al., 2017 source
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Every source the paper cites for this claim was checked and supports it.
In the paper
“Greater NDI than controls was observed in subcortical WM adjacent to regions of reduced ODI.”
§ NODDI in clinical research > 3.14. Effects of drugs and substance abuse
What the sources say
- Supportedcites Morris et al., 2018 source
The Results (Neurite orientation dispersion and density) report higher white-matter neurite density adjacent to lower grey-matter ODI in binge drinkers, including in the right dorsolateral prefrontal cortex. The paper calls this adjacent tissue “cortical white matter”; the claim’s “subcortical WM” describes its location beneath the cortex. (LLM, conf=0.88)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“earlier studies were partly inconsistent regarding the changes of NDI and ODI (Billiet et al., 2015;Chang et al., 2015;Kodiweera et al., 2016;Merluzzi et al., 2016), possibly reflecting heterogeneity in the age ranges investigated in these studies.”
§ NODDI in clinical research > 4.1. Normal development and aging: late childhood to old age
What the sources say
- Not checked — no full text of the sourcecites Billiet et al., 2015 source
- Partly supportedcites Chang et al., 2015 sourceExperimental — accuracy not yet measured
The Results (section 3.2; page unavailable) report age-related NDI and ODI trajectories, so Chang et al. is an earlier study relevant to the comparison. The Discussion (section 4.4; page unavailable) says its smaller older group biases those trajectories toward development. The paper does not itself establish that the cited studies had inconsistent findings or that differences in their age ranges explain the inconsistency. (LLM, conf=0.78)
- Supportedcites Kodiweera et al., 2016 source
In Discussion > Aging effects (page unavailable), the paper describes mixed findings for age-related ICVF changes in earlier studies, reports no significant ICVF change in its young-to-middle-aged cohort, and contrasts its ODI finding with Billiet et al. It suggests that population differences may help explain the ODI discrepancy, consistent with the citing sentence’s hedged explanation. (LLM, conf=0.86)
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesThe cited sources support only part of this claim — read each source’s verdict below.
In the paper
“although neither NODDI nor DKI have shown a particular benefit over DTI in predicting isocitrate dehydrogenase-1 gene mutation status (Figini et al., 2018;Zhao et al., 2018).”
§ NODDI in clinical research > 3.11. Brain tumors
What the sources say
- Supportedcites Figini et al., 2018 source
The Discussion (p. 5) says the benefit of advanced diffusion models was small and that DTI identified IDH status as well as multishell methods. The Summary (p. 2) likewise says advanced models did not add significant diagnostic accuracy. The Neuropathologic Examination (p. 3) specifies that IDH-1 mutation status was assessed. (LLM, conf=0.90)
- Partly supportedcites Zhao et al., 2018 sourceExperimental — accuracy not yet measured
The Results section reports no significant overall difference in NODDI or DTI metrics between patients with and without IDH-1 mutations, supporting the limited claim about NODDI. But it also reports a significant NODDI finding in grade IV gliomas. The paper does not test whether DKI offers a benefit over DTI for predicting mutation status, so that part of the claim is unsupported by this source. (LLM, conf=0.88)
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In the paper
“With NODDI applied postoperatively, NDI showed a positive correlation with neurological score at the time of MRI (Jiang et al., 2018;Ma et al., 2018).”
§ NODDI in clinical research > 3.12. Spondylotic myelopathy
What the sources say
- Supportedcites Jiang et al., 2018 source
The Introduction identifies Vic (intracellular volume fraction) as the NODDI measure of neurite density. The Results report a positive correlation between postoperative Vic and the follow-up mJOA neurological score (r = 0.420, p = 0.001). The paper calls the score a follow-up measure rather than explicitly saying it was obtained at the time of MRI. (LLM, conf=0.90)
- Not matchedcites Ma et al., 2018
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Although an increase of f fw with age has been consistently observed”
§ NODDI in clinical research > 4.1. Normal development and aging: late childhood to old age
What the sources say
- Partly supportedcites Cox et al., 2016 sourceExperimental — accuracy not yet measured
The Results report higher ISOVF with older age, and the Discussion says this agrees with prior estimates from middle to older age. The paper describes ISOVF as a measure of extracellular water diffusion, but does not identify it as the specific f_fw measure or establish a consistent increase across all ages. No page numbers are available in our copy. (LLM, conf=0.82)
- Not checked — no full text of the sourcecites Guerreri et al., 2019 source
- Supportedcites Merluzzi et al., 2016 source
The Introduction defines Viso as the fraction of a voxel occupied by isotropically diffusing, CSF-like water. The Results report widespread age-related increases in Viso, and the Discussion says a previous study observed similar increases. The finding is regional rather than universal, but it supports the cited statement that an increase has been observed consistently. (LLM, conf=0.88)
Strength:boosted· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“With NODDI, the T2-weighted hyperintense lesion of gliomas exhibit a smaller NDI and greater f fw compared with normal-appearing WM (Lampinen et al., 2017;Maximov et al., 2017;Wen et al., 2015).”
§ NODDI in clinical research > 3.11. Brain tumors
What the sources say
- Partly supportedcites Lampinen et al., 2017 sourceExperimental — accuracy not yet measured
The Fig. 5 caption reports generally higher free-water fractions and mostly lower anisotropic-water fractions in gliomas than in normal tissue. It also notes that NODDI’s f_IC parameter was elevated in parts of the tumors. The paper does not establish the claim specifically for T2-hyperintense lesions compared with normal-appearing white matter, and the unqualified lower-NDI statement omits those exceptions. (LLM, conf=0.85)
- Not checked — no full text of the sourcecites Maximov et al., 2017 source
- Supportedcites Wen et al., 2015 source
The Results (Evaluation of NODDI parameters; page not supplied) report significantly decreased intra-neurite volume fraction (vic) and increased isotropic volume fraction (viso) in T2-weighted lesions compared with normal-appearing white matter. The Methods identify these as the restricted and free-water-related NODDI compartments, respectively. (LLM, conf=0.91)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“(Cox et al., 2016) and (Slater et al., 2019) have consistently found that among the dMRI parameters (FA, MD, NDI, ODI, and f fw ) MD is the most sensitive to the effect of aging.”
§ NODDI in clinical research > 4.1. Normal development and aging: late childhood to old age
What the sources say
- Partly supportedcites Cox et al., 2016 sourceExperimental — accuracy not yet measured
The Discussion reports that MD was the most sensitive conventional dMRI or NODDI parameter to age among the thalamic radiations and association fasciculi studied. The claim omits that tract-specific scope and the study’s middle-to-older-age population, making it broader than the finding in our copy. (LLM, conf=0.84)
- Not checked — no full text of the sourcecites Slater et al., 2019 source
Strength:boosted· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In patients undergoing interferon alpha therapy, (Dowell et al., 2019) found that increased NDI in the left striatum compared with baseline was associated with the occurrence of fatigue.”
§ NODDI in clinical research > 3.14. Effects of drugs and substance abuse
What the sources say
- Supportedcites Dowell et al., 2019 source
The Results section (‘Relationship with change in fatigue’) reports a significant positive correlation between acute changes in NDI and fatigue in the left striatum. The paper measured NDI at baseline and again four hours after the first IFN-α dose, matching the claim’s comparison. (LLM, conf=0.94)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Besides, accelerated computation via convex optimization (Daducci et al., 2015) is available for NODDI.”
§ NODDI in clinical research > 5.2. Toward a clinical tool
What the sources say
- Supportedcites Daducci et al., 2015 source
The NODDI section states that the authors’ convex formulation provides estimates for the NODDI model. It reports that fitting the synthetic data took about 40 hours with the original algorithm versus 6 minutes with the convex NODDI amico approach, directly supporting accelerated computation via convex optimization. (LLM, conf=0.95)
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In a rat model co-expressing TAR DNA-binding protein 43 and toxic variants of tau, none of the NODDI parameters showed significant differences from controls, despite pathological evidence of microglial activation (Moszczynski et al., 2019).”
§ NODDI in clinical research > 5.3. Specificity beyond NODDI
What the sources say
- Supportedcites Moszczynski et al., 2019 source
The Results > Neuroimaging section reports no differences between groups in the corpus callosum or hippocampus for the NODDI measures ODI, NDI, and IsoVF. The Results > Tau pathology in rats section reports significantly increased IBA1 staining, a marker of microglial activation, in rats co-expressing TDP-43M337V and tauT175D relative to controls. The claim is supported for the brain regions and measures examined. (LLM, conf=0.94)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Several studies (Billiet et al., 2015(Billiet et al., , 2014;;Fenchel et al., 2020;Geeraert et al., 2019;Hara et al., 2019;Slater et al., 2019) have demonstrated the benefits of combining NODDI with other complementary imaging methods to allow for more specific inferences about the underlying microstructure.”
§ NODDI in clinical research > 5.1. Summary of clinical studies
What the sources say
- Not checked — no full text of the sourcecites Billiet et al., 2015 source
- Partly supportedcites Fenchel et al., 2020 sourceExperimental — accuracy not yet measured
The Image Processing and MSN Construction methods describe combining NODDI-derived measures with other diffusion and structural MRI measures. The Discussion says the combination captures information no single measure captures, but the paper demonstrates richer characterization of neonatal cortical patterns, not specifically more precise inferences about the underlying microstructure. Page numbers are not available in our copy. (LLM, conf=0.83)
- Not checked — no full text of the sourcecites Geeraert et al., 2019 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesThe cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Children born very preterm exhibit greater ODI throughout the WM at the age of 6-7 years compared with full-term children (Kelly et al., 2016;Young et al., 2019).”
§ NODDI in clinical research > 4.3. Developmental abnormalities
What the sources say
- Partly supportedcites Kelly et al., 2016 sourceExperimental — accuracy not yet measured
The Methods (MRI acquisition; page unavailable) place the scans at age 7, and the Discussion (VPT children compared with controls; page unavailable) reports increased axon dispersion in many white-matter tracts in very preterm children. The paper does not establish greater dispersion throughout all white matter; that wording is broader than its reported finding. (LLM, conf=0.87)
- Supportedcites Young et al., 2019 source
The Discussion reports widespread increases in ODI in children born very preterm compared with term-born children at six years of age. In the citing sentence, Young et al. supports the six-year-old portion of the stated 6–7-year age range. (LLM, conf=0.90)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Recently, in a large cohort of term-born infants, both NDI and ODI in the cortex were found to be positively correlated with gestational age at 37-44 weeks (Fenchel et al., 2020).”
§ NODDI in clinical research > 4.2. Normal development and aging: perinatal to childhood
What the sources say
- Partly supportedcites Fenchel et al., 2020 sourceExperimental — accuracy not yet measured
The Results (Age at Scan and Sex Effects) report positive associations of cortical NDI and ODI with age in a cohort of term-born infants. But the Subjects section defines the 37–44-week range as postmenstrual age at scanning, not gestational age at birth; infants were born at 37–42 weeks. (LLM, conf=0.89)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Applications of NODDI in the presence of neuroinflammation have reported mixed results so care should be taken in interpreting the relationship between NODDI and neuroinflammation.”
§ NODDI in clinical research > 5.3. Specificity beyond NODDI
What the sources say
- Partly supportedcites Dowell et al., 2019 sourceExperimental — accuracy not yet measured
The Results and Discussion (page not available in our copy) report mixed findings within this IFN-α study: no significant group-level change in NODDI metrics, but a positive correlation between striatal NDI changes and fatigue. The Discussion also cautions that factors other than inflammation can affect NDI. The paper does not establish that NODDI applications across neuroinflammatory settings have generally reported mixed results. (LLM, conf=0.83)
- Partly supportedcites Moszczynski et al., 2019 sourceExperimental — accuracy not yet measured
The Results (Tau pathology in rats; page unavailable) report increased hippocampal microglial activation in one rat group, while the Results (Neuroimaging; page unavailable) report no group differences in NODDI measures. This supports caution about interpreting NODDI alongside neuroinflammation, but the paper does not report mixed results across NODDI applications. (LLM, conf=0.78)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“NODDI was also shown to be sensitive to individual variations of WM microstructure at 1 month of age that are associated with prenatal maternal depression and anxiety symptoms (Dean et al., 2018).”
§ NODDI in clinical research > 4.3. Developmental abnormalities
What the sources say
- Supportedcites Dean et al., 2018 source
The paper says it evaluated white matter microstructure in 1-month-old infants using NODDI. Its Results report that prenatal maternal depression and anxiety symptoms were associated with decreased neurite-density measures, particularly in frontal white matter. No page number is available in our copy. (LLM, conf=0.92)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Also, NDI in the posterior callosal connections showed a negative correlation with reading skill (Huber et al., 2019).”
§ NODDI in clinical research > 4.3. Developmental abnormalities
What the sources say
- Supportedcites Huber et al., 2019 source
In Results (‘Biological underpinnings of reading-diffusion correlations’; page unavailable), NODDI ICVF significantly correlates with reading skill, and struggling readers tend to have higher ICVF throughout the posterior callosal tract. The paper calls this measure ICVF rather than NDI; its reported direction supports the claimed negative correlation. (LLM, conf=0.90)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In children with developmental dyslexia, ODI and NDI in the language-related cortical regions were correlated with a measure of gyrification in opposite directions from typically developing controls”
§ NODDI in clinical research > 4.3. Developmental abnormalities
What the sources say
- Supportedcites Caverzasi et al., 2018 source
The Results section (‘Relationship between gyrification, neurite density and fiber dispersion’; page not provided) reports opposite slopes for children with developmental dyslexia and typically developing controls: ODI versus local gyrification index (lGI) in the left rostral middle frontal gyrus, and NDI versus lGI in the left middle temporal gyrus. These are the language-related frontal and temporal regions described in the claim. (LLM, conf=0.94)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Widespread reduction of NDI in WM was also present in young adults born with congenital heart disease (Easson et al., 2020).”
§ NODDI in clinical research > 4.3. Developmental abnormalities
What the sources say
- Supportedcites Easson et al., 2020 source
The Conclusion (section 4.5) reports widespread NDI reductions in many white matter tracts in youth born with congenital heart disease compared with healthy controls. The study population was aged 16–24 years (Study design), consistent with the citing sentence’s description of young adults. (LLM, conf=0.93)
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Pathologies like axonal beading/swelling (Budde and Frank, 2010;Palombo et al., 2018) and demyelination (Chuhutin et al., 2020;Guglielmetti et al., 2016;Jelescu et al., 2016) also affect compartmental diffusivities.”
§ NODDI in clinical research > 5.3. Specificity beyond NODDI
What the sources say
- Not checked — no full text of the sourcecites Budde and Frank, 2010 source
- Not checked — no full text of the sourcecites Palombo et al., 2018 source
- Partly supportedcites Chuhutin et al., 2020 sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) reports that extra-axonal parallel diffusivity increased with EAE grade and proposes myelin loss as one possible explanation. It does not establish that demyelination itself caused the change; axonal damage and glial changes are also proposed. The axonal beading/swelling portion is attached to other citations, not this one. (LLM, conf=0.83)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesThe sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Recently proposed extensions of NODDI to measurements with b-tensor encoding (Guerreri et al., 2020) and with multiple TE (Gong et al., 2020) showed capability of estimating compartmental diffusivities and T2s using clinical scanners, and we may see some confirmations and/or re-interpretations of the previously-reported NODDI findings in near future.”
§ NODDI in clinical research > 5.3. Specificity beyond NODDI
What the sources say
- Not checked — no full text of the sourcecites Guerreri et al., 2020
- Supportedcites Gong et al., 2020 source
Gong et al. is cited for the multiple-TE extension. The Introduction describes estimating compartment-specific T2 values from multiple-TE diffusion data, and Methods §3.1.1 reports an in vivo demonstration on a Siemens 3T scanner. The separate b-tensor citation, rather than Gong et al., is attached to the other extension in the sentence. (LLM, conf=0.88)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesEvery source the paper cites for this claim was checked and supports it.
In the paper
“An important limitation of MRI g-ratio is that any bias introduced by the individual participating models or by the procedure to compute the g-ratio is propagated into the final output in an unpredictable way (Campbell et al., 2018).”
§ NODDI in clinical research > 5.4. Combination of multiple contrasts
What the sources say
- Supportedcites Campbell et al., 2018 source
Section 3.3.3 (pp. 11–12) says that inaccurate calibration of the myelin estimate makes the computed g-ratio incorrect and can introduce a misleading dependence on fiber density. Section 3.1 (p. 5) also describes preprocessing errors that produce artifactually high or otherwise incorrect g-ratios. These passages support the claim that biases in the component estimates or computation carry through to the final metric, with effects that depend on the source of error. (LLM, conf=0.87)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Disentangling these factors beyond NODDI is expected to further improve our understanding of the brain and diseases, just as NODDI revealed the putative neuronal damage beyond limitations of DTI in diseases like Alzheimer's disease (Slattery et al., 2017) and iNPH (Kamiya et al., 2017).”
§ NODDI in clinical research > 5.3. Specificity beyond NODDI
What the sources say
- Supportedcites Slattery et al., 2017 source
The Introduction explains that DTI gives a composite view of tissue microstructure, whereas NODDI can distinguish neurite-density loss from changes in axonal organization. The Discussion reports that, in young-onset Alzheimer’s disease, NODDI enabled more specific inferences about damage and could reveal effects not observable as a DTI fractional-anisotropy change. The separate iNPH example is attributed to Kamiya et al., not to this source. (LLM, conf=0.92)
- Supportedcites Kamiya et al., 2017 source
The Introduction says conventional DTI measures are not highly specific to individual microstructural properties. In the iNPH study, the Abstract and Conclusion report lower estimated axon density that persisted after surgery, suggesting a marker of irreversible neuronal damage. The paper attributes this finding to both NODDI and WMTI, consistent with the citing sentence’s claim about NODDI in iNPH. (LLM, conf=0.90)
Strength:hedged· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“At present, consensus has not been reached even on the very basic assumptions such as the number of compartments.”
§ NODDI in clinical research > 2.2. Is NODDI specific?
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In contrast, biophysical models such as NODDI align with the second reason-to provide better explanations for observed abnormalities-by increasing specificity for certain clinically meaningful tissue properties.”
§ NODDI in clinical research > 2. Rationale for using NODDI in clinical research
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn the paper
“The choice of fixed parallel diffusivity value (1.7 µm /ms 2 ) was based on minimization of the fitting residuals for voxels in the corpus callosum (Alexander et al., 2010).”
§ NODDI in clinical research > 2.1. The NODDI model
What the sources say
- Not checked — no full text of the sourcecites Alexander et al., 2010 source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIn the paper
“As shown in the original work by (Zhang et al., 2012), NODDI is more specific than fractional anisotropy (FA) in DTI, in that voxels with different sets of NODDI parameters can yield exactly the same FA value and therefore be indistinguishable by FA.”
§ NODDI in clinical research > 2.2. Is NODDI specific?
What the sources say
- Not checked — no full text of the sourcecites Zhang et al., 2012 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn the paper
“Although there is no easy answer (Novikov et al., 2018a), a simple reply is that it depends on purpose and that the specificity of NODDI is only relative.”
§ NODDI in clinical research > 2.2. Is NODDI specific?
What the sources say
- Not matchedcites Novikov et al., 2018a
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Not matched
In the paper
“Lower FA and NDI, and higher mean diffusivity (MD) and ODI, were associated with worse neuropsychological scores (Q.Wen et al., 2019b).”
§ NODDI in clinical research > 3.1. Alzheimer's disease
What the sources say
- Not matchedcites Q.Wen et al., 2019b
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Not matched
In the paper
“ODI in GM generally exhibits a greater CoV than it does in WM, which is expected because estimation of higher ODI values are less precise (Zhang et al., 2012).”
§ NODDI in clinical research > 2.3. Is NODDI reliable?
What the sources say
- Not checked — no full text of the sourcecites Zhang et al., 2012 source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“suggests the presence of different microstructural mechanisms at the different disease stages (e.g., neuroinflammation occurs early, followed by neurodegeneration)”
§ NODDI in clinical research > 3.1. Alzheimer's disease
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesThe paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“This nonmonotonic course, which is characterized by a stronger diffusion restriction at an intermediate amyloid burden and a weaker diffusion restriction at a higher burden, suggests the presence of different microstructural mechanisms at the different disease stages (e.g., neuroinflammation occurs early, followed by neurodegeneration), and so future longitudinal studies with methods that allow”
§ NODDI in clinical research > 3.1. Alzheimer's disease
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn the paper
“and interscanner reproducibility has been shown to be lower than intra-scanner reproducibility, even at the same field strength (3 T) (Andica et al., 2019b).”
§ NODDI in clinical research > 2.3. Is NODDI reliable?
What the sources say
- Not matchedcites Andica et al., 2019b
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Not matched
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Also, assuming multiple Gaussian compartments means we neglect several potentially important factors, including inter-compartmental exchange and non-Gaussian effects within the compartments.”
§ NODDI in clinical research > 2.2. Is NODDI specific?
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“indicating that NODDI has the ability, at least partly, to disentangle the effect of orientation dispersion.”
§ NODDI in clinical research > 2.2. Is NODDI specific?
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesThe paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Despite that, NODDI can describe multi-shell dMRI data better than DTI, illustrating the benefit of well-crafted model suitable for acquisition.”
§ NODDI in clinical research > 2.2. Is NODDI specific?
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn the paper
“Reduced NDI in WM has also been reported in pre-symptomatic carriers of c9orf72 mutation, a major genetic cause of ALS (J.Wen et al., 2019a).”
§ NODDI in clinical research > 3.4. Amyotrophic lateral sclerosis
What the sources say
- Not matchedcites J.Wen et al., 2019a
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Not matched
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“In addition, NDI and ODI in the putamen was negatively correlated with motor symptom severity and disease duration, which is in agreement with the clinico-pathological hypothesis that striatal dendrite degeneration contributes to late-stage motor symptoms in Parkinson's disease (Zaja-Milatovic et al., 2005).”
§ NODDI in clinical research > 3.2. Parkinson's disease
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn the paper
“In GM, decreased NDI and increased f fw within the striatum and the frontal, temporal, limbic, and paralimbic cortices have been identified before atrophy is evident (Kamagata et al., 2017).”
§ NODDI in clinical research > 3.2. Parkinson's disease
What the sources say
- Not checked — no full text of the sourcecites Kamagata et al., 2017 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesThe paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“In contrast, changes in ODI have been reported in all directions-as increases, decreases, or as no significant changes.”
§ NODDI in clinical research > 3.3. Multiple sclerosis
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIn the paper
“Later, a larger case series (Rostampour et al., 2018) also reported that NODDI was useful for the visual detection of FCDs.”
§ NODDI in clinical research > 3.5. Epilepsy
What the sources say
- Not checked — no full text of the sourcecites Rostampour et al., 2018 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Animal studies have shown a progressive decrease of NDI in the brain (Gatto et al., 2019) and spinal cord (Gatto et al., 2018) of ALS mice, and these findings were in good agreement with histologically measured decreases of the intra-axonal space.”
§ NODDI in clinical research > 3.4. Amyotrophic lateral sclerosis
What the sources say
- Not checked — no full text of the sourcecites Gatto et al., 2019 source
- Not checked — no full text of the sourcecites Gatto et al., 2018
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Increases of ODI and f fw were also observed in these mice.”
§ NODDI in clinical research > 3.4. Amyotrophic lateral sclerosis
What the sources say
- Not checked — no full text of the sourcecites Gatto et al., 2019 source
- Not checked — no full text of the sourcecites Gatto et al., 2018
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIn the paper
“Also, (Yasuno et al., 2019) found that ODI in the left posterior cingulate cortex was associated with the severity and recovery of post-stroke depression”
§ NODDI in clinical research > 3.6. Ischemia
What the sources say
- Not checked — no full text of the sourcecites Yasuno et al., 2019 source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIn the paper
“In DTI, patients with iNPH exhibit greater FA within the CST compared with controls (Hattingen et al., 2010)”
§ NODDI in clinical research > 3.9. Idiopathic normal pressure hydrocephalus
What the sources say
- Not checked — no full text of the sourcecites Hattingen et al., 2010 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn the paper
“a higher ODI in the corpus callosum (Spray et al., 2018a) and lower ODI in the left superior temporal gyrus (Spray et al., 2018b) were reported to be associated with proneness to auditory hallucination.”
§ NODDI in clinical research > 3.10. Schizophrenia
What the sources say
- Not matchedcites Spray et al., 2018b
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Not matched
In the paper
“a higher ODI in the corpus callosum (Spray et al., 2018a) and lower ODI in the left superior temporal gyrus (Spray et al., 2018b) were reported to be associated with proneness to auditory hallucination.”
§ NODDI in clinical research > 3.10. Schizophrenia
What the sources say
- Not matchedcites Spray et al., 2018a
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Not matched
In the paper
“(Espay et al., 2017) pointed out that the initial diagnoses of iNPH were revised later in more than 25 % of the patients (revised diagnosis: Alzheimer's disease, dementia with Lewy bodies, or progressive supranuclear palsy).”
§ NODDI in clinical research > 3.9. Idiopathic normal pressure hydrocephalus
What the sources say
- Not checked — no full text of the sourcecites Espay et al., 2017 source
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“and a few studies have reported a trend of partial normalization after surgery (Jurcoane et al., 2014;Scheel et al., 2012).”
§ NODDI in clinical research > 3.9. Idiopathic normal pressure hydrocephalus
What the sources say
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIn the paper
“In auto-pedestrian accidents, a widespread reduction of NDI in WM shortly after trauma has been reported (Wu et al., 2018).”
§ NODDI in clinical research > 3.7. Traumatic brain injury
What the sources say
- Not matchedcites Wu et al., 2018
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Not matched
In the paper
“A smaller NDI in the frontotemporal cortices was linked with lower neurocognitive performance (Nazeri et al., 2017).”
§ NODDI in clinical research > 3.10. Schizophrenia
What the sources say
- Not checked — no full text of the sourcecites Nazeri et al., 2017 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn the paper
“During these processes, myelin plays important roles related to axon vulnerability (Armstrong et al., 2016).”
§ NODDI in clinical research > 3.7. Traumatic brain injury
What the sources say
- Not checked — no full text of the sourcecites Armstrong et al., 2016 source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIn the paper
“WM damage in TBI is histopathologically characterized by axonal swelling at the initial damage, followed by axonal degeneration, demyelination, and neuroinflammation with microglial activation (Armstrong et al., 2016).”
§ NODDI in clinical research > 3.7. Traumatic brain injury
What the sources say
- Not checked — no full text of the sourcecites Armstrong et al., 2016 source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIn the paper
“With NODDI, a smaller NDI was found in GM regions such as the temporal pole, anterior parahippocampal gyrus, and hippocampus in patients with schizophrenia compared with healthy controls (Nazeri et al., 2017).”
§ NODDI in clinical research > 3.10. Schizophrenia
What the sources say
- Not checked — no full text of the sourcecites Nazeri et al., 2017 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Although all imaging techniques are inevitably dependent on simplistic models and are limited in their specificity, combining complementary techniques allows us to deduce the biological underpinnings of diseases beyond the limitation of a single model.”
§ NODDI in clinical research > 3.8. Neurofibromatosis type 1
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn the paper
“Recently, another large-sample life span study including participants aged 7-84 years (Slater et al., 2019) identified 'U-shaped' or 'inverted U-shaped' life span trajectories in NODDI parameters”
§ NODDI in clinical research > 4.1. Normal development and aging: late childhood to old age
What the sources say
- Not checked — no full text of the sourcecites Slater et al., 2019 source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“suggesting that the relationship between cortical ODI and neurocognitive decline with age is likely not straightforward.”
§ NODDI in clinical research > 4.1. Normal development and aging: late childhood to old age
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIn the paper
“The trends observed by (Cox et al., 2016) and (Slater et al., 2019) agree with the 'last in, first out' hypothesis (Bartzokis, 2004)”
§ NODDI in clinical research > 4.1. Normal development and aging: late childhood to old age
What the sources say
- Not checked — no full text of the sourcecites Bartzokis, 2004 source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIn the paper
“Survivors of childhood bone and soft tissue sarcoma, on average at 10 years after chemotherapy, exhibited widespread areas with greater f fw compared with controls in central WM, presumably representing interstitial edema (Sleurs et al., 2018).”
§ NODDI in clinical research > 3.14. Effects of drugs and substance abuse
What the sources say
- Not checked — no full text of the sourcecites Sleurs et al., 2018 source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“DKI's mean kurtosis is known to correlate well with tumor grade (Raab et al., 2010;Van Cauter et al., 2012)”
§ NODDI in clinical research > 3.11. Brain tumors
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“In preoperative evaluation, greater NDI at the level of strongest compression was associated with greater neurological recovery after surgery (Iwama et al., 2020;Okita et al., 2018).”
§ NODDI in clinical research > 3.12. Spondylotic myelopathy
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn the paper
“Greater NDI in the frontal cortex was observed in patients undergoing lithium therapy compared with patients treated with other mood stabilizers (Sarrazin et al., 2019)”
§ NODDI in clinical research > 3.14. Effects of drugs and substance abuse
What the sources say
- Not checked — no full text of the sourcecites Sarrazin et al., 2019 source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIn the paper
“does not necessarily mean recovered axon density, as shown in a post-mortem case report where the pathological change of spinal cord persisted after surgery and did not coincide with the relief of symptoms (Someya et al., 2011).”
§ NODDI in clinical research > 3.12. Spondylotic myelopathy
What the sources say
- Not checked — no full text of the sourcecites Someya et al., 2011 source
Strength:plain· not yet calibratedSingle caseTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIn the paper
“In contrast, in breast cancer survivors, no significant difference from healthy controls was observed at 3-4 years after the end of chemotherapy (Billiet et al., 2018).”
§ NODDI in clinical research > 3.14. Effects of drugs and substance abuse
What the sources say
- Not checked — no full text of the sourcecites Billiet et al., 2018 source
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“It is unlikely that computational cost is the main reason, because current medical practice spends a long time on image processing, for example, during surgical planning.”
§ NODDI in clinical research > 5.2. Toward a clinical tool
Strength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“There are also many other factors that are not mathematically parameterized in NODDI but could be biologically meaningful.”
§ NODDI in clinical research > 5.3. Specificity beyond NODDI
Strength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesThe paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“One of the major concerns about dMRI microstructure models is that they have not yet been adopted for clinical use.”
§ NODDI in clinical research > 5.2. Toward a clinical tool
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesThe paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Interpretations of NODDI depend on the clinical condition under examination and our associated biological hypotheses.”
§ NODDI in clinical research > 5.3. Specificity beyond NODDI
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesThe paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Compared with the case of apparent diffusion coefficient and dMRI tractography, the pace of dissemination has been relatively slow.”
§ NODDI in clinical research > 5.2. Toward a clinical tool
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In the presence of intercompartmental differences in the relaxation times, compartmental fractions estimated via NODDI can be influenced by alterations of both actual volumes and relaxation times.”
§ NODDI in clinical research > 5.3. Specificity beyond NODDI
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Although each study is meaningful as a proof-of-concept, at present it is difficult to draw general conclusions about the practical benefit of NODDI in individual patient care.”
§ NODDI in clinical research > 5.1. Summary of clinical studies
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes? Checkable: unclear✓ Load-bearing: passes✓ Based: passes
- Probably not a substantial claim. 52
- It may state two separate claims as one. 73
At least one cited source doesn’t support this claim or points to a different paper, and none confirmed it — see the verdicts below.
In the paper
“A very recent report (Guerreri et al., 2020) suggested that the fixed diffusivity assumption, but not the tortuosity model, is the primary cause of NODDI's incompatibility with b-tensor encoding (Lampinen et al., 2017).”
§ NODDI in clinical research > 2.2. Is NODDI specific?
What the sources say
- Not checked — no full text of the sourcecites Guerreri et al., 2020
- Disputedcites Lampinen et al., 2017 sourceExperimental — accuracy not yet measured
Section 2.3 describes the fixed neurite diffusivity and the tortuosity model as linked NODDI constraints, not competing explanations. Sections 4.3 and 5 attribute the LTE–STE inconsistency to invalid constraints connecting neurite density with tissue mean diffusivity. The paper therefore does not support excluding tortuosity as a cause. (LLM, conf=0.84)
Checked by a reasoning model — may be wrong.
Strength:hedged· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“There are two main approaches to extracting information from dMRI data: signal representations and biophysical models (Jelescu and Budde, 2017;Jespersen, 2018;Novikov et al., 2018a).”
§ NODDI in clinical research > 1. Introduction
What the sources say
- Supportedcites Jelescu and Budde, 2017 source
Section 1 (Models) explicitly identifies two complementary approaches to extracting information from the diffusion signal: signal representations and tissue models. Section 1.4 (Summary) calls these signal representations and biophysical models, while noting that hybrid models combine features of both. (LLM, conf=0.94)
- Not checked — no full text of the sourcecites Jespersen, 2018 source
- Not matchedcites Novikov et al., 2018a
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Recent years have seen a marked proliferation of biophysical models with the explicit aim of clinically feasible data acquisition (single-diffusion encoding, b-values up to 2000-3000 s/mm 2 , diffusion time 20-100 ms) (Fieremans et al., 2011;Hansen et al., 2017;Kaden et al., 2016;Zhang et al., 2012).”
§ NODDI in clinical research > 1. Introduction
What the sources say
- Supportedcites Fieremans et al., 2011 source
The Introduction identifies DKI combined with a tissue model as a clinically feasible alternative to models requiring high b-values or long scans. Methods §2.2.2 reports acquisition at b-values up to 2000 s/mm² and a diffusion time of about 50 ms; Discussion §4.2 emphasizes the model’s shorter acquisition time and clinical usefulness. This paper supports the citation as an example of a biophysical model designed for clinically feasible acquisition, rather than as evidence of proliferation on its own. (LLM, conf=0.87)
- Supportedcites Hansen et al., 2017 source
The Discussion (page unavailable) describes a faster WMTI approach that reduces the number of images required and says it may be useful in clinical settings where scan time is constrained. The human-brain Methods (page unavailable) report single-diffusion encoding, b-values up to 3.0 ms/μm² (3000 s/mm²), and a diffusion time of approximately 50 ms. This paper therefore supports its role as an example of a biophysical approach designed for clinically feasible acquisition; it does not need to establish the broader trend of proliferation on its own. (LLM, conf=0.90)
- Supportedcites Kaden et al., 2016 source
This citation serves as an example of a biophysical model designed for clinically feasible acquisition, rather than as evidence for the number of models developed. The Abstract describes a multi-compartment model usable within clinically feasible scan times; Clinical translation specifies a roughly five-minute, two-shell protocol at b-values of 1000 and 2500 s/mm². Human data describes a Stejskal–Tanner acquisition with a 43.1 ms pulse separation, within the cited diffusion-time range. (LLM, conf=0.91)
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In clinical research, diffusion tensor imaging (DTI) (Basser et al., 1994) has long been an important tool that has yielded many insights in a wide range of neurological and psychological disorders (for recent reviews see (Andica et al., 2019a;Goveas et al., 2015;Pasternak et al., 2018).”
§ NODDI in clinical research > 1. Introduction
What the sources say
- Not matchedcites Andica et al., 2019a
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked — no full text of the sourcecites Goveas et al., 2015 source
- Partly supportedcites Pasternak et al., 2018 sourceExperimental — accuracy not yet measured
The Introduction reports DTI findings in schizophrenia, bipolar disorder, and major depressive disorder, supporting its value in psychiatric research. It says the review is limited to those conditions, so this source does not establish the claim about a wide range of neurological disorders. (LLM, conf=0.84)
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Similar repeatability is also reported in the cervical spinal cord (By et al., 2017;Grussu et al., 2015;Ma et al., 2018), although a greater CoV for ODI and f fw has been observed in GM, reflecting the general challenges of dMRI in the spinal cord (e.g., small structure, magnetic field inhomogeneity, cerebrospinal fluid pulsation and physiological noise).”
§ NODDI in clinical research > 2.3. Is NODDI reliable?
What the sources say
- Not matchedcites By et al., 2017
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Supportedcites Grussu et al., 2015 source
The Results (§3.2.2, page not available in our copy) report reproducibility in the cervical spinal cord and higher coefficients of variation in gray matter than white matter for both ODI (44% versus 7%) and the isotropic volume fraction, v_iso (140% versus 41%). The paper uses v_iso for the isotropic compartment, corresponding to the claim’s free-water fraction notation. (LLM, conf=0.90)
- Not matchedcites Ma et al., 2018
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Not matched
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“f fw is less stable than NDI and ODI, with a scan-rescan CoV of 10 %-40 % (Andica et al., 2019b;Chung et al., 2016;Granberg et al., 2017).”
§ NODDI in clinical research > 2.3. Is NODDI reliable?
What the sources say
- Not matchedcites Andica et al., 2019b
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Partly supportedcites Chung et al., 2016 sourceExperimental — accuracy not yet measured
The Results (Within-Session Reproducibility; page unavailable) say that νiso, the free-water fraction, had the largest within-session CV, supporting its lower stability relative to NDI and ODI. The paper does not give a 10%–40% scan-rescan CV for νiso in the available text. The Discussion instead gives a 3.8%–40% range for between-subject NODDI CV and explicitly excludes νiso from that range. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites Granberg et al., 2017 source
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Not matched
Every source the paper cites for this claim was checked and supports it.
In the paper
“In the GM of patients with young-onset Alzheimer's disease, reductions of NDI and ODI were found in the temporal cortex and precuneus, and a smaller NDI in the cortex was associated with more severe cognitive impairment (Parker et al., 2018).”
§ NODDI in clinical research > 3.1. Alzheimer's disease
What the sources say
- Supportedcites Parker et al., 2018 source
The Results report lower NDI and ODI in the inferior and middle temporal gyri and precuneus of young-onset Alzheimer’s patients than in controls. The Discussion reports that lower NDI in those regions was associated with a lower MMSE cognition score. (LLM, conf=0.93)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Several studies (Fukutomi et al., 2018;Genç et al., 2018) found optimizing d i, based on the fitting residual is helpful for re- vealing cortical cytoarchitecture with NODDI, though their method is still dependent on the assumption of equal diffusivities ( = d d i, e, ).”
§ NODDI in clinical research > 2.2. Is NODDI specific?
What the sources say
- Supportedcites Fukutomi et al., 2018 source
In Materials and Methods (NODDI and DTI calculation; page unavailable), the authors select an optimized diffusivity using model fit to cortical data. The Discussion (Cortical neurite properties resemble microscopic findings and cortical classifications; page unavailable) links the resulting NODDI measures to cortical cytoarchitecture, while the Discussion (Optimization and validity of NODDI in the gray matter; page unavailable) explicitly retains the assumption of equal intracellular and extracellular axial diffusivity. The paper describes fit quality using maximum likelihood rather than the term “fitting residual,” but the substantive attribution matches. (LLM, conf=0.88)
- Partly supportedcites Genç et al., 2018 sourceExperimental — accuracy not yet measured
The Methods section (“Analysis of imaging data in the S259 sample”; page unavailable) says the authors adjusted NODDI’s intrinsic free-diffusivity parameter to 1.1 × 10−3 mm²/s for gray matter to analyze cortical structure. It does not say they selected that value by minimizing fitting residuals or state the claimed assumption of equal intra- and extra-neurite diffusivities. (LLM, conf=0.85)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“With NODDI, (Slattery et al., 2017) reported reduced NDI in the parieto-occipital WM in both ε4+ and ε4-patients with young-onset Alzheimer's disease relative to controls, with the reduction more widespread in ε4+ patients.”
§ NODDI in clinical research > 3.1. Alzheimer's disease
What the sources say
- Supportedcites Slattery et al., 2017 source
The Results section (“White-matter structural differences by APOE ε4 genotype”) states that NDI was reduced in parieto-occipital white-matter projections in both ε4− and ε4+ young-onset Alzheimer’s disease groups relative to controls, and that the reduction was more widespread in ε4+ patients. It also notes that direct comparisons between the patient groups did not reach the prescribed statistical threshold. (LLM, conf=0.95)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Also, even within usual multi-shell acquisition (linear tensor encoding), the optimal value of d i, seems different between neonates and adults, as well as between white matter (WM) and gray matter (GM) (Guerrero et al., 2019).”
§ NODDI in clinical research > 2.2. Is NODDI specific?
What the sources say
- Supportedcites Guerrero et al., 2019 source
The Discussion reports that both age and tissue type affect the optimal intrinsic parallel diffusivity in the multi-shell diffusion MRI data studied. The Conclusion states that the optimum is near the default value in adult white matter, but lower in adult gray matter and in both white and gray matter of the newborn brain. The supplied passages do not explicitly use the term “linear tensor encoding,” but they support the attributed age- and tissue-dependent finding. (LLM, conf=0.91)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Though extended acquisitions have been proposed toward unconstrained estimation of the model parameters (Lampinen et al., 2020 et al., 2018b;Veraart et al., 2018), at present, the increased scan time hampers clinical application of these cutting-edge techniques.”
§ NODDI in clinical research > 2.2. Is NODDI specific?
What the sources say
- Supportedcites Lampinen et al., 2020 source
The citation is attached to the proposal of extended acquisitions for less-constrained parameter estimation. The Results (Sampling protocols and parameter precision; page unavailable) describe an optimized 10-shell protocol, and the Methods (In vivo acquisition and processing; page unavailable) report a 15-minute, multi-TE acquisition. The statement that scan time hampers clinical application follows the citation and is the citing authors’ framing, not a finding attributed to this paper. (LLM, conf=0.88)
- Supportedcites Veraart et al., 2018 source
The Methods describe varying both b-values and TE to estimate diffusion and relaxation parameters simultaneously, and the Results discuss parameter estimation without imposed constraints. The Discussion (Optimal design) says the densely sampled, one-hour protocol has limited value in a clinical setting. (LLM, conf=0.90)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“(Slattery et al., 2017) also demonstrated improved sensitivity of NODDI over DTI, reporting parallel reductions of NDI and ODI in some WM regions that had no observable changes in FA.”
§ NODDI in clinical research > 3.1. Alzheimer's disease
What the sources say
- Supportedcites Slattery et al., 2017 source
The Results section (Fig. 3B and accompanying text) reports parallel NDI and ODI reductions in a right frontal white-matter region of patients with young-onset Alzheimer’s disease, despite no significant FA change. It explicitly describes NODDI metrics as more sensitive than FA in this setting because the opposing effects cancel in FA. (LLM, conf=0.94)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The validity of such constraints is a matter of debate, even in the normal brain, with several works (Lampinen et al., 2020(Lampinen et al., , 2017;;Novikov et al., 2018b) pointing out incompatibility of NODDI with extended data acquisitions.”
§ NODDI in clinical research > 2.2. Is NODDI specific?
What the sources say
- Supportedcites Lampinen et al., 2020 source
The Theory section identifies equal axial diffusivities and the tortuosity relation as constraints used by NODDI. The In vivo results report that estimates from the richer acquisition contradicted these commonly enforced relations and that the unconstrained model fit most regions of the healthy brain significantly better than models enforcing equal T2 values or tortuosity. Page numbers are unavailable in our copy. (LLM, conf=0.92)
- Supportedcites Lampinen et al., 2017 source
The Introduction says NODDI's model constraints had not been experimentally validated and proposes comparing LTE with STE data. The Discussion reports that the constraints appear invalid in the brain: STE-based neurite-density maps did not resemble LTE-based maps, and the gray-matter fit was relatively poor. This supports the attributed concern even in the healthy brain when the acquisition is extended to STE. (LLM, conf=0.94)
- Not matchedcites Novikov et al., 2018b
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“When applied to clinical studies, the use of different constraints sometimes yields results that agree in their relative trends (Huber et al., 2019;Jelescu et al., 2015;Kamiya et al., 2017), but such agreement is not always guaranteed and is not proof of validity.”
§ NODDI in clinical research > 2.2. Is NODDI specific?
What the sources say
- Partly supportedcites Huber et al., 2019 sourceExperimental — accuracy not yet measured
The Results (Biological underpinnings of reading-diffusion correlations; page unavailable) report that measures from two models, NODDI and WMTI, both correlated with reading skill in children, supporting an example of agreement in relative trends. The paper does not establish that differing model constraints generally yield agreement across clinical studies. The caution after the citations is not clearly attributed to Huber et al. (LLM, conf=0.82)
- Supportedcites Jelescu et al., 2015 source
Section 4.1.2 reports relative agreement between WMTI and NODDI in age-related trends, but substantially different quantitative estimates and poorer agreement for some parameters. Sections 5.3 and 2.3 explain that the models’ assumptions can bias those estimates, so agreement in trends does not establish validity. (LLM, conf=0.90)
- Supportedcites Kamiya et al., 2017 source
The Introduction says NODDI and WMTI use different constraints and that the authors compared them for consistency. The Discussion reports consistent findings despite different estimated values, while cautioning that the models have intrinsic limitations and the results require careful interpretation. The paper provides an example of agreement in trends, not a guarantee of agreement or proof of validity. (LLM, conf=0.88)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In a mouse model of tau pathology, NDI in WM and hippocampus was reduced, and NDI in GM was positively correlated with the level of hyperphosphorylated tau protein (Colgan et al., 2016).”
§ NODDI in clinical research > 3.1. Alzheimer's disease
What the sources say
- Partly supportedcites Colgan et al., 2016 sourceExperimental — accuracy not yet measured
The Results (Hippocampus and Corpus callosum; page unavailable) report lower NDI in the tau-model mice, supporting the reduction in hippocampus and white matter. The Results (Cortex and Hippocampus; page unavailable) report correlations between NDI and tau burden in grey matter, but do not establish the claimed positive direction; they report higher cortical NDI but lower hippocampal NDI in the model mice. (LLM, conf=0.86)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In temporal lobe epilepsy (TLE), the most common epilepsy in adults, reduction of NDI was found in the temporal lobes, with more prominent abnormalities in the hemisphere ipsilateral to the epileptogenic focus (Sone et al., 2018;Winston et al., 2020).”
§ NODDI in clinical research > 3.5. Epilepsy
What the sources say
- Supportedcites Sone et al., 2018 source
The Introduction (page not provided) calls TLE the most common type of adult epilepsy. The Results and Conclusions (pages not provided) report reduced neurite density mainly in the ipsilateral temporal lobe in both left and right TLE, supporting the claimed hemispheric pattern. (LLM, conf=0.94)
- Supportedcites Winston et al., 2020 source
The Results (Intracortical grey matter; page unavailable) report reduced neurite density confined to ipsilateral mesial and basal temporal regions. The Results (Subcortical white matter; page unavailable) report bilateral neurite-density reductions, alongside stronger ipsilateral effects for a related diffusion measure. Together, these support reduced temporal-lobe neurite density with more prominent ipsilateral abnormalities, although the paper does not explicitly quantify an ipsilateral-versus-contralateral difference in neurite density. (LLM, conf=0.87)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“(Winston et al., 2014) reported that NDI maps yielded a clearer depiction of FCD than other imaging approaches (i.e., T1-/T2-weighted images and DTI maps).”
§ NODDI in clinical research > 3.5. Epilepsy
What the sources say
- Supportedcites Winston et al., 2014 source
The Results state that reduced ICVF, the NODDI measure of neurite density, was more conspicuous than on conventional structural or diffusion images. The Discussion likewise says the abnormality was more readily identifiable than on other clinical or diffusion images, supporting the comparison with T1-/T2-weighted and DTI imaging. (LLM, conf=0.91)
Load-bearingStrength:boosted· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In postmortem human spinal cord, (Grussu et al., 2017) observed decreased ODI in MS lesions and an excellent agreement between ODI and its histological counterpart.”
§ NODDI in clinical research > 3.3. Multiple sclerosis
What the sources say
- Supportedcites Grussu et al., 2017 source
The Results section reports decreased ODI in a thoracic MS lesion and a trend toward decreased ODI in lumbar lesions. Its statistical analysis reports a strong correlation between ODI and its histological counterpart, CV, in MS cases (r = 0.60; P = 0.001), supporting the described agreement. (LLM, conf=0.88)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The potential usefulness of NODDI for discriminating Parkinson's disease from the other Parkinsonian disorders has also been suggested (Mitchell et al., 2019), with NODDI showing greater abnormalities in progressive supranuclear palsy and multiple system atrophy than in Parkinson's disease.”
§ NODDI in clinical research > 3.2. Parkinson's disease
What the sources say
- Supportedcites Mitchell et al., 2019 source
The Differentiation of Parkinsonism section reports that NODDI distinguished PD from atypical Parkinsonism (the studied MSAp and PSP groups), with an AUC of 0.945. The Introduction describes more widespread pathological changes in MSAp and PSP than in PD, and the NODDI results identify abnormalities across multiple regions in those groups. The study examined the Parkinsonian variant of multiple system atrophy, rather than all variants. (LLM, conf=0.86)
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“They also reported that reduced NDI was seen in larger areas than was FA, suggesting a greater sensitivity of NODDI over DTI, and that reduced ODI within the precentral gyrus was correlated with disease duration, presumably representing reduced dendritic density and branching.”
§ NODDI in clinical research > 3.4. Amyotrophic lateral sclerosis
What the sources say
- Supportedcites Broad et al., 2019 source
The Discussion reports that, at the same statistical threshold, significantly reduced NDI covered larger areas than significantly reduced FA. It explicitly suggests that NDI may be more sensitive than FA for detecting ALS-related white-matter pathology. (LLM, conf=0.94)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“These studies generally agree that NDI in WM is reduced compared with healthy controls in MR-visible lesions, and to a lesser degree in normal-appearing WM, and that NDI reveals more prominent and widespread abnormalities than FA (Fig. 4).”
§ NODDI in clinical research > 3.3. Multiple sclerosis
What the sources say
- Not matchedcites Collorone et al., 2019
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Partly supportedcites De Santis et al., 2019 sourceExperimental — accuracy not yet measured
The Effect size section reports reduced NODDI restricted fraction in MS lesions and normal-appearing white matter, while FA differences did not survive the post-hoc test. This supports the comparison with FA, but the claim is too broad across protocols: the NODDI difference in normal-appearing white matter was not significant at 7 T. The paper does not establish that the abnormalities were more widespread beyond the tissue regions it tested. (LLM, conf=0.87)
- Not checked — no full text of the sourcecites Granberg et al., 2017 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Not matched
Every source the paper cites for this claim was checked and supports it.
In the paper
“Tractography and network analysis both have their own limitations (Jeurissen et al., 2019;Sotiropoulos and Zalesky, 2019), which, in combination with the limitations of NODDI, means that caution is required when interpreting the data.”
§ NODDI in clinical research > 3.5. Epilepsy
What the sources say
- Supportedcites Jeurissen et al., 2019 source
Jeurissen's discussion accompanying Figure 14 says fiber-tracking connectomes can contain false positives, false negatives, and biased connection strengths, and advises proceeding with extreme caution. The citation supports the tractography limitation in the citing sentence; that sentence does not attribute the limitations of network analysis or NODDI specifically to Jeurissen. (LLM, conf=0.93)
- Supportedcites Sotiropoulos and Zalesky, 2019 source
The citation is attached to the statement that tractography and network analysis have limitations, not to the separate mention of NODDI. In “Mapping edges,” the paper describes tractography errors and urges caution; in “Comparing network properties between groups,” it says interpreting brain graphs is challenging and some network measures rest on unestablished assumptions. (LLM, conf=0.92)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The tuberous sclerosis patients also exhibited smaller NDI compared with controls throughout the WM, although no correlation was observed with severity of mental retardation or epilepsy.”
§ NODDI in clinical research > 3.5. Epilepsy
What the sources say
- Partly supportedcites Taoka et al., 2020 sourceExperimental — accuracy not yet measured
The Results (Quantitative analysis; page unavailable) report reduced Ficv, a measure of neurite density, across widespread white-matter regions—not throughout all white matter. The Results (Correlations of clinical symptoms; page unavailable) found no statistically significant correlations with mental retardation or epilepsy, although the Discussion describes slight associations with mental-retardation severity. (LLM, conf=0.85)
Strength:plain· not yet calibratedn = 11Tests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“NDI in this region was not different from the contralateral side in the subacute phase, and was decreased in the chronic phase, presumably representing the course of Wallerian degeneration (Mastropietro et al., 2019).”
§ NODDI in clinical research > 3.6. Ischemia
What the sources say
- Supportedcites Mastropietro et al., 2019 source
The Discussion (page unavailable) reports no significant ipsilateral–contralateral difference in Fic, the paper’s intraneurite NODDI measure, in the subacute phase. The chronic-phase Results (page unavailable) report significantly lower ipsilateral Fic in the distal CST region (CP), and the Discussion describes the changes as compatible with Wallerian degeneration. (LLM, conf=0.92)
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Notably, (Sone et al., 2018) observed reduced NDI in patients with TLE in whom experienced radiologists did not find abnormalities on structural MRI, albeit to a lesser extent than in patients with MRI-positive TLE (Fig. 5).”
§ NODDI in clinical research > 3.5. Epilepsy
What the sources say
- Supportedcites Sone et al., 2018 source
The Participants section (page unavailable) says experienced neuroradiologists assessed the MRI scans and found no conventional-MRI abnormalities in the MRI-negative/PET-positive group. The Results and Discussion (page unavailable) report reduced neurite density in that group, with less severe abnormalities than in the MRI-positive TLE group with hippocampal sclerosis. (LLM, conf=0.93)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“In addition, increased f fw in the substantia nigra, which is consistent with accumulated evidence (Burciu et al., 2017(Burciu et al., , 2016) ) from free water imaging (Pasternak et al., 2009), was observed by (Mitchell et al., 2019) but not by (Kamagata et al., 2016).”
§ NODDI in clinical research > 3.2. Parkinson's disease
What the sources say
- Supportedcites Mitchell et al., 2019 source
Section 3.4 (page not provided) reports elevated free water in the posterior substantia nigra in Parkinson’s disease, MSAp, and PSP compared with controls. This supports the finding attributed to Mitchell et al.; the separate claim about Kamagata et al. is not assessed against Mitchell’s paper. (LLM, conf=0.93)
- Not checked — no full text of the sourcecites Kamagata et al., 2016 source
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Interestingly, a study of the long-term effects of sports-related concussion reported increased NDI and decreased ODI in athletes at 9-120 months after their last concussion compared with controls”
§ NODDI in clinical research > 3.7. Traumatic brain injury
What the sources say
- Supportedcites Churchill et al., 2017 source
The Subject Demographics section reports that athletes were imaged 9 months to 10 years after their last concussion. The Discussion reports increased intracellular volume fraction (VIC), indicating greater neurite density, and decreased ODI in concussed athletes compared with controls. Page numbers are not available for these passages. (LLM, conf=0.92)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In patients with moyamoya disease, a disease characterized by progressive occlusion of the circle of Willis, NODDI parameters in GM and WM were correlated with hemodynamic activities measured with 15 O-gas positron-emission tomography, as well as neurocognitive dysfunction”
§ NODDI in clinical research > 3.6. Ischemia
What the sources say
- Not checked — no full text of the sourcecites Hara et al., 2019 source
- Partly supportedcites Hara et al., 2018 sourceExperimental — accuracy not yet measured
The Conclusions (page unavailable) report a correlation between NODDI and neuropsychological performance in adult moyamoya disease, and describe white-matter and cortical NODDI differences. The Statistical Analysis section (page unavailable) describes correlations with cognitive scores, but our copy does not report a correlation between NODDI parameters and hemodynamic activity measured by 15O-gas PET. (LLM, conf=0.86)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
Every source the paper cites for this claim was checked and supports it.
In the paper
“After surgery, the orientation parameter showed partial normalization, whereas the reduced axonal water fraction remained unchanged (Kamiya et al., 2017) (Fig. 7).”
§ NODDI in clinical research > 3.9. Idiopathic normal pressure hydrocephalus
What the sources say
- Supportedcites Kamiya et al., 2017 source
The Results (Human data) report that the orientation parameter τ1 decreased significantly after surgery and that neither imaging model found a significant postoperative change in axonal water fraction (AWF). The Discussion describes the increased orientational coherence as tending to normalize while the decreased axon density remained unchanged. (LLM, conf=0.93)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Furthermore, individuals with a history of TBI are at higher risk for dementia, neurodegenerative diseases, psychiatric illness, and even mortality, indicating long-term progression of sub-clinical pathology that manifests only in late adulthood (Smith et al., 2013;Wilson et al., 2017).”
§ NODDI in clinical research > 3.7. Traumatic brain injury
What the sources say
- Partly supportedcites Smith et al., 2013 sourceExperimental — accuracy not yet measured
The Introduction and “Single TBI” section support increased risk of later dementia and neurodegenerative disease, particularly after moderate to severe TBI. “Repetitive mild TBI” reports neuropsychiatric symptoms in selected cases and higher neurodegenerative mortality in former NFL players, but does not establish a general increased risk of psychiatric illness or mortality for everyone with a TBI history. The “Histological features” section also describes pathology appearing within hours of injury, so the claim that it manifests only in late adulthood is not supported. (LLM, conf=0.87)
- Partly supportedcites Wilson et al., 2017 sourceExperimental — accuracy not yet measured
The sections on neurodegenerative disease after single TBI and stroke and other neurological disorders after TBI report links with dementia, neurodegenerative disease, and neuropsychiatric illness; the Conclusions and future directions report higher mortality. But the paper does not establish that these outcomes all result from sub-clinical pathology manifesting only in late adulthood: it describes that mechanism as a possibility and also reports young-onset dementia and elevated mortality in younger people. No page numbers are available in our copy. (LLM, conf=0.86)
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The degree of post-operative improvement varies greatly among individuals, and therefore quantitative metrics capable of predicting treatment response have been sought (Halperin et al., 2015).”
§ NODDI in clinical research > 3.9. Idiopathic normal pressure hydrocephalus
What the sources say
- Supportedcites Halperin et al., 2015 source
The Abstract reports differing outcomes among shunted patients, including marked or moderate improvement in 14 of 18 patients and minimal worsening in one. The Conclusion and Figure 2 discuss measured CSF flow, outflow resistance, and other tests assessed for their ability to predict shunt response. Together, these support the paraphrase. (LLM, conf=0.88)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“No significant differences were observed for ODI, f fw , myelin water fraction, or intra-or extra-neurite water fraction.”
§ NODDI in clinical research > 3.8. Neurofibromatosis type 1
What the sources say
- Partly supportedcites Billiet et al., 2014 sourceExperimental — accuracy not yet measured
The dMRI Results report no significant differences in ODI or isotropic fluid fraction (FISO), and the multi-exponential T2 Results report none in myelin water fraction or combined intra- and extracellular water fraction (IEWF). The comparison is specifically between unidentified bright objects and normal-appearing white matter in children with NF1. The paper does not report separate intra- or extra-neurite water fractions; calling its combined IEWF measure those fractions is not supported. (LLM, conf=0.88)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“With NODDI, axonal water fraction and orientation dispersion were both smaller within the CST of patients”
§ NODDI in clinical research > 3.9. Idiopathic normal pressure hydrocephalus
What the sources say
- Supportedcites Kamiya et al., 2017 source
The Results (Human data; page unavailable) report significantly lower NODDI axonal water fraction in the CST of iNPH patients than controls, alongside higher τ1, indicating greater orientational coherence. The Image processing section (page unavailable) defines higher τ1 as more parallel orientation, supporting the claim of lower orientation dispersion. (LLM, conf=0.92)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Studies have suggested that, depending on their anatomical location (e.g., thalamus), UBOs may be associated with cognitive deficits (Hyman et al., 2007;Moore et al., 1996).”
§ NODDI in clinical research > 3.8. Neurofibromatosis type 1
What the sources say
- Supportedcites Hyman et al., 2007 source
The Results state that T2 hyperintensities were not associated with cognitive dysfunction overall, but thalamic lesions were associated with cognitive impairment. The Location of T2H section reports lower cognitive scores in children with thalamic lesions, while lesions in several other locations showed no significant lowering. This supports the claim's location-dependent, hedged association. (LLM, conf=0.94)
- Not checked — no full text of the sourcecites Moore et al., 1996 source
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“the observed NDI increase has been interpreted as representing the inflammatory process.”
§ NODDI in clinical research > 3.14. Effects of drugs and substance abuse
What the sources say
- Could not verifycites Haroon et al., 2014 sourceExperimental — accuracy not yet measured
The Abstract and Discussion report increased glutamate measured as Glu/Cr during IFN-alpha treatment and discuss possible inflammatory mechanisms. Our copy does not report an NDI increase or interpret NDI as representing inflammation (searched: NDI, neurite density index). (LLM, conf=0.76)
- Not checked — no full text of the sourcecites Capuron et al., 2007 source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Could not verify
Every source the paper cites for this claim was checked and supports it.
In the paper
“In WM, NDI has a positive correlation with age, but the increase is non-linear and more rapid during early life (Dean et al., 2016;Jelescu et al., 2015;Lynch et al., 2020) (Fig. 9B).”
§ NODDI in clinical research > 4.2. Normal development and aging: perinatal to childhood
What the sources say
- Supportedcites Dean et al., 2016 source
The Methods identify νIC as the NODDI measure of neurite density. The Results (Fig. 4; page not provided) report that mean white-matter νIC increases logarithmically with age in the study’s infants and young children, supporting a nonlinear increase that is faster earlier in life. (LLM, conf=0.92)
- Supportedcites Jelescu et al., 2015 source
The Results (§4.1, page unavailable) report that the NODDI-derived intra-axonal fraction increased in all three white-matter regions during the first three years of life and that an exponential curve best described the increase. The Conclusion (§6, page unavailable) likewise describes a large nonlinear increase with age and notes that the trajectory levels off, supporting a faster increase early in the period studied. (LLM, conf=0.90)
- Supportedcites Lynch et al., 2020 source
The Discussion reports widespread age-related increases in white-matter tract NDI. It describes an exponential growth pattern, with rapid increases in infancy and young childhood followed by a plateau in adolescence. (LLM, conf=0.94)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Although DTI has consistently shown reduced FA in the compressed spinal cord, the correlation of FA with symptoms and postoperative recovery remains controversial (Jones et al., 2013;Rajasekaran et al., 2017).”
§ NODDI in clinical research > 3.12. Spondylotic myelopathy
What the sources say
- Partly supportedcites Jones et al., 2013 sourceExperimental — accuracy not yet measured
The Correlation with Initial Clinical Assessment Scores section reports lower FA with poorer neurologic function in patients with cervical spondylotic myelopathy. The Relation to Surgical Outcome section reports an association between baseline FA and improvement on one postoperative measure, but not on the Nurick or mJOA scales; the Conclusions call the results preliminary. This supports uncertainty about postoperative prediction, but the paper does not establish that correlations with symptoms and recovery are broadly controversial or that reduced FA has been shown consistently across studies. (LLM, conf=0.85)
- Not checked — no full text of the sourcecites Rajasekaran et al., 2017 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“However, (Genç et al., 2018) have reported that higher intelligence in healthy young to middle-aged individuals was associated with lower cortical ODI”
§ NODDI in clinical research > 4.1. Normal development and aging: late childhood to old age
What the sources say
- Supportedcites Genç et al., 2018 source
The Results (Associations on a whole-brain level; page not provided) report a negative association between intelligence and cortical ODI in both samples. The same section describes participants aged 18–40 and 22–36, and the Methods describe the experimental sample as healthy. (LLM, conf=0.93)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Reduced ODI in the frontal cortices and increased ODI in the parietal cortices and the striatum have been reported from a study in young-adult binge drinkers (Morris et al., 2018).”
§ NODDI in clinical research > 3.14. Effects of drugs and substance abuse
What the sources say
- Supportedcites Morris et al., 2018 source
The Discussion reports reduced ODI in frontal cortical grey matter and increased ODI in parietal cortex in young-adult binge drinkers. It also reports higher ODI in the ventral striatum; the Results section confirms this comparison with healthy volunteers. (LLM, conf=0.91)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Another study found that lower NDI in WM was associated with poorer mathematics performance-but not with reading performance-across children born very preterm and full term (Collins et al., 2019).”
§ NODDI in clinical research > 4.3. Developmental abnormalities
What the sources say
- Supportedcites Collins et al., 2019 source
The Results (Associations between white matter microstructure and mathematics; page not available) report that higher neurite density was associated with better mathematics performance in the combined VPT and FT sample. The Results (Associations between white matter microstructure and word reading; page not available) report no association between any measured diffusion parameter and word reading performance in that sample. (LLM, conf=0.93)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“For example, in patients receiving interferon alpha treatment in whom an inflammatory cytokine response was confirmed by blood test, ODI remained unchanged, although NDI was increased (Dowell et al., 2019).”
§ NODDI in clinical research > 5.3. Specificity beyond NODDI
What the sources say
- Partly supportedcites Dowell et al., 2019 sourceExperimental — accuracy not yet measured
The Results sections on inflammatory cytokine response and acute NODDI effects report a blood-measured cytokine response and no significant change in ODI. However, they also report no significant increase in NDI after IFN-α; most of the listed NDI means were slightly lower at 4 hours. (LLM, conf=0.90)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Compared with controls, infants with congenital heart disease exhibited smaller NDI and greater ODI in WM (Karmacharya et al., 2018), as well as smaller ODI in cortical GM (Kelly et al., 2019)”
§ NODDI in clinical research > 4.3. Developmental abnormalities
What the sources say
- Supportedcites Karmacharya et al., 2018 source
The Results section (‘White matter regional abnormalities in CHD’; page unavailable) reports lower NODDI intracellular volume fraction (Vic) in the bilateral SFOF and left PLIC, and higher ODI in the left corpus callosum, in CHD neonates compared with controls. These are region-specific white-matter findings. The cortical-gray-matter claim is attached to Kelly et al. (2019), not to this source. (LLM, conf=0.90)
- Supportedcites Kelly et al., 2019 source
The Results section ('Cortical ODI Is Reduced in Infants With CHD') reports significantly lower cortical ODI in infants with congenital heart disease than in controls. Kelly et al. is cited for the cortical gray matter finding, not the white matter findings attributed to Karmacharya et al. (LLM, conf=0.94)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Both lower NDI and greater ODI were correlated with poorer neurodevelopmental outcomes (Kelly et al., 2016;Mürner-Lavanchy et al., 2018;Young et al., 2019).”
§ NODDI in clinical research > 4.3. Developmental abnormalities
What the sources say
- Supportedcites Kelly et al., 2016 source
The Discussion’s Conclusions state that higher axon dispersion (ODI) and lower axon density (NDI) in very preterm children are associated with some neurodevelopmental delays. The Neurodevelopmental outcomes section also links both measures to poorer motor outcomes. (LLM, conf=0.91)
- Supportedcites Mürner-Lavanchy et al., 2018 source
The Discussion reports that higher axon density was associated with better IQ and motor performance and fewer behavioural problems, while lower axon dispersion was associated with better motor performance and fewer behavioural problems in very-preterm children. It also reports higher axon density with better semantic performance in this study, although evidence for dispersion–language associations was weaker. Those findings support the broad claim about poorer neurodevelopmental outcomes; the motor and behavioural findings are reported from earlier work. (LLM, conf=0.88)
- Partly supportedcites Young et al., 2019 sourceExperimental — accuracy not yet measured
The Discussion reports that, among children born very preterm, lower NDI was associated with poorer intelligence and visuomotor skills, but intelligence was associated with NDI rather than ODI. Greater ODI was associated with lower intellectual scores in the full-term group; in that group, higher—not lower—NDI was also associated with lower scores. The claim combines associations observed in different groups as though both applied together. (LLM, conf=0.90)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Focusing on the fixed diffusivity assumption, (Guerrero et al., 2019) have suggested that the default value of 1.7 μm 2 /ms is likely suboptimal for neonates brain and GM, and that the age-dependence of NDI and ODI is affected by the choice of fixed diffusivity value.”
§ NODDI in clinical research > 4.2. Normal development and aging: perinatal to childhood
What the sources say
- Supportedcites Guerrero et al., 2019 source
The Results report that the optimal fixed diffusivity is below 1.7 μm²/ms in infant white and gray matter, and in gray matter across age groups. The Results and Discussion also show that changing this value alters age-group differences in neurite density and orientation-related NODDI parameters. The copy provides section labels but no page numbers. (LLM, conf=0.93)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Accumulating evidence suggests a major role of chronic neuroinflammation in the neurodegeneration that occurs in aging and in a broad range of diseases including Alzheimer's disease, Parkinson's disease, MS, ALS, stroke, TBI, and psychiatric diseases (Amor et al., 2010;Glass et al., 2010;Vikhreva et al., 2016).”
§ NODDI in clinical research > 5.3. Specificity beyond NODDI
What the sources say
- Partly supportedcites Amor et al., 2010 sourceExperimental — accuracy not yet measured
The Abstract and Conclusions describe chronic immune activation as a feature of many neurodegenerative diseases, and the paper discusses the listed neurological conditions, including ALS. The Introduction mentions an aging population but does not establish a role for chronic neuroinflammation in neurodegeneration caused by aging; the passages found also do not address psychiatric diseases. Page numbers are unavailable in our copy. (LLM, conf=0.88)
- Partly supportedcites Glass et al., 2010 sourceExperimental — accuracy not yet measured
The Introduction and Conclusion support a role for sustained neuroinflammation in the progression of Alzheimer’s, Parkinson’s, ALS, and MS, while noting that inflammation may amplify pathology rather than initiate disease. The Alzheimer’s Disease section identifies AD as age-related, but the cited passages do not establish the broader claim about neurodegeneration in aging, stroke, traumatic brain injury, or psychiatric diseases. Page numbers are unavailable in our copy. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites Vikhreva et al., 2016 source
Strength:hedged· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“For example, T2s are likely different among compartments (Lampinen et al., 2020;Veraart et al., 2018) and are affected by pathologies like neuroinflammation (Stanisz et al., 2004), demyelination (Bartzokis, 2004;Lin et al., 2018), and intramyelinic edema (Harkins et al., 2013).”
§ NODDI in clinical research > 5.3. Specificity beyond NODDI
What the sources say
- Supportedcites Lampinen et al., 2020 source
The Lampinen et al. citation is attached to the claim that T2 values differ among compartments, not to the subsequent examples of pathologies, which have separate citations. The Results (In vivo results; page not provided) report different T2 values for the ‘stick’ and ‘zeppelin’ compartments in both healthy white matter and lesions. (LLM, conf=0.94)
- Supportedcites Veraart et al., 2018 source
Veraart et al. is cited for the first clause, that T2 values differ among compartments. The Discussion reports empirical evidence that intra- and extra-axonal T2 relaxation times differ, and the Conclusion reiterates this finding in the living human brain. The pathology examples have separate citations and are not attributed to Veraart et al. (LLM, conf=0.94)
- Not checked — no full text of the sourcecites Stanisz et al., 2004 source
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Although the negative correlation may look counterintuitive, it is in line with a number of studies reporting higher FA within this region in individuals with reading difficulties and the hypothesis that left lateralization of reading-related functions is diminished in struggling readers (Dougherty et al., 2007;Finn et al., 2014).”
§ NODDI in clinical research > 4.3. Developmental abnormalities
What the sources say
- Not checked — no full text of the sourcecites Dougherty et al., 2007 source
- Partly supportedcites Finn et al., 2014 sourceExperimental — accuracy not yet measured
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
Every source the paper cites for this claim was checked and supports it.
In the paper
“For translation into the clinic, an imaging biomarker needs to pass multiple steps in three parallel tracks: technical validation (precision, accuracy, and realizability), biological/clinical validation (performance in measuring relevant biological properties or predicting clinical outcomes), and cost-effectiveness (Connor et al., 2017).”
§ NODDI in clinical research > 5.2. Toward a clinical tool
What the sources say
- Supportedcites Connor et al., 2017 source
The imaging biomarker roadmap section describes parallel technical and biological/clinical validation tracks, with cost-effectiveness as a third track considered as validation evidence accumulates. It specifies precision, accuracy and availability for technical performance, and measurement of relevant biology or prediction of clinical outcomes for biological/clinical performance. The cost-effectiveness section says clinical translation requires good value for money. (LLM, conf=0.91)
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Later, (Batalle et al., 2019) reported that cortical development between 25 and 38 weeks is dominated by an increase of ODI, whereas between 38 and 47 weeks it is dominated by an increase of NDI”
§ NODDI in clinical research > 4.2. Normal development and aging: perinatal to childhood
What the sources say
- Supportedcites Batalle et al., 2019 source
The Discussion describes increases in ODI before 38 weeks PMA, followed by increased NDI with no change in ODI after 38 weeks. The Abstract gives the same 25–38 and 38–47 week pattern, while noting that later NDI increases were regionally confined. (LLM, conf=0.91)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Preliminary applications of NODDI and the g-ratio framework include studies of brain maturation during childhood (Dean et al., 2016;Geeraert et al., 2019), the effects of age and gender in young-to-late adulthood (Berman et al., 2018;Cercignani et al., 2017;Slater et al., 2019), and the effects of diseases like MS (Hagiwara et al., 2019;Stikov et al., 2015;Yu et al., 2019) and cervical spondylotic”
§ NODDI in clinical research > 5.4. Combination of multiple contrasts
What the sources say
- Supportedcites Dean et al., 2016 source
Dean et al. is cited for the childhood-maturation example, not the separately cited adult or disease studies. The Discussion reports a preliminary NODDI-based g-ratio study in children and a developmental trajectory across infancy and early childhood; page numbers are not provided in our copy. (LLM, conf=0.93)
- Not checked — no full text of the sourcecites Geeraert et al., 2019 source
- Supportedcites Berman et al., 2018 source
Berman et al. is an application of the g-ratio framework to age and sex: Methods §2.1 reports participants aged 7–85, and §2.5 describes testing sex differences across age ranges. The Conclusions state that the study tested g-ratio stability with age and between the sexes. The citing sentence identifies the subject of the study; it does not claim that the study found significant age or sex effects. (LLM, conf=0.92)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“A few studies have adopted this type of multi-parameter analysis with NODDI (Andica et al., 2020;Churchill et al., 2019Churchill et al., , 2017)), although most have been limited to combinations with other dMRI measures.”
§ NODDI in clinical research > 5.4. Combination of multiple contrasts
What the sources say
- Partly supportedcites Andica et al., 2020 sourceExperimental — accuracy not yet measured
The Methods (Linked independent component analysis) confirm that this study combined NODDI with DTI and VBM measures in a multi-parameter analysis. Because VBM measures white-matter volume, this study was not limited to other dMRI measures; the cited paper also does not establish that most such studies were so limited. (LLM, conf=0.85)
- Not checked — no full text of the sourcecites Churchill et al., 2019 source
- Supportedcites Churchill et al., 2017 source
The Magnetic Resonance Imaging section describes a protocol estimating both DTI and NODDI parameters. The Multivariate analysis: effects of concussion section says the study used N-way Partial Least Squares to examine covariation across multiple diffusion MRI measures and concussion history. This supports citing the paper as an example of multi-parameter NODDI analysis combined with another dMRI measure; the paper does not establish how common that approach is across other studies. (LLM, conf=0.91)
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Several groups have been even more ambitious and have investigated the use of MRI g-ratio as weights in connectomics studies (Kamagata et al., 2019;Mancini et al., 2018).”
§ NODDI in clinical research > 5.4. Combination of multiple contrasts
What the sources say
- Supportedcites Kamagata et al., 2019 source
The Introduction says the authors mapped connectomes based on the MR g-ratio in patients with multiple sclerosis. The Methods describe their g-ratio-weighted connectivity matrices, directly supporting the use of MRI g-ratio as connectome weights. (LLM, conf=0.94)
- Supportedcites Mancini et al., 2018 source
Section 2.4.2 (‘G-ratio weighted networks’) says the study modelled connectome edges with the g-ratio itself as their weight. This supports citing Mancini et al. as one group that investigated MRI g-ratio weights in connectomics; it does not need to establish what the other cited group did. (LLM, conf=0.94)
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“One rapidly growing field is joint modeling of diffusion and relaxation (Gong et al., 2020;Lampinen et al., 2020;Veraart et al., 2018) (see also Hutter et al. in this special issue).”
§ NODDI in clinical research > 5.4. Combination of multiple contrasts
What the sources say
- Supportedcites Gong et al., 2020 source
The Introduction (page unavailable) describes combined modelling of diffusion and T2 relaxation and traces its development into more recent imaging methods. The Discussion (page unavailable) says an early study inspired many techniques and gives recent examples, supporting the broad characterization of a growing field. (LLM, conf=0.86)
- Supportedcites Lampinen et al., 2020 source
The Introduction (page unavailable) treats diffusion-relaxation experiments as an active research approach, describing their use to estimate compartment-specific T2 values and citing several recent studies. The paper itself develops a joint diffusion-relaxation model, supporting its citation as an example of this growing field. (LLM, conf=0.84)
- Supportedcites Veraart et al., 2018 source
The Introduction describes the paper’s own approach as combining diffusion and relaxation in a biophysical model. It also points to a vast literature on joint diffusion–relaxation methods and recent extensions to imaging, supporting the citing sentence’s broad characterization of an active, growing field. (LLM, conf=0.87)
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“As with other advanced imaging techniques, most of the disease studies reported to date have been cross-sectional and have included a sample of limited size from a single center.”
§ NODDI in clinical research > 5.1. Summary of clinical studies
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“In contrast, biophysical models aim at specificity by parametrizing the dMRI signal as a function of biophysically meaningful parameters (e.g., axon density).”
§ NODDI in clinical research > 1. Introduction
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“There are two main reasons for introducing a new imaging technique to the study of a disease: to improve sensitivity to target pathologies and to provide better explanations for observed abnormalities.”
§ NODDI in clinical research > 2. Rationale for using NODDI in clinical research
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“As the models are often based on assumptions that are not yet proven even in the normal brain, users must be aware of the risk of being misled in their interpretations of the data.”
§ NODDI in clinical research > 2. Rationale for using NODDI in clinical research
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✗ Based: failsProbably not a substantial claim. The paper may give no reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The validity of model assumptions is currently under debate.”
§ NODDI in clinical research > 2.2. Is NODDI specific?
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The signal representation approach aligns with the first reason, to improve sensitivity to target pathologies, with the caveat that this approach comes with no obvious biological interpretation.”
§ NODDI in clinical research > 2. Rationale for using NODDI in clinical research
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“neurite orientation dispersion and density imaging (NODDI) has been proposed as a way to relate the dMRI signal to tissue features via biophysically inspired modeling.”
§ NODDI in clinical research > Abstract
What the sources say
- Not checked — no full text of the sourcecites Zhang et al., 2012 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
In the paper
“With NODDI, reduced NDI and ODI have been observed in the substantia nigra and putamen of patients with Parkinson's disease compared with controls, and these reductions were predominant on the side corresponding to symptoms (contralateral) (Kamagata et al., 2016).”
§ NODDI in clinical research > 3.2. Parkinson's disease
What the sources say
- Not checked — no full text of the sourcecites Kamagata et al., 2016 source
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Despite the remaining ambiguity about model assumptions, research to investigate the clinical usefulness of NODDI can still be justified.”
§ NODDI in clinical research > 2.2. Is NODDI specific?
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✗ Checkable: fails✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may be too vague to check against evidence.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“NODDI may provide useful biomarkers if the effect of disease is far greater than the bias introduced by the constraints.”
§ NODDI in clinical research > 2.2. Is NODDI specific?
Tests✓ Asserted: passes✗ Checkable: fails✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may be too vague to check against evidence.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“As the one true model has not been identified, results of NODDI, and any other model, are more or less phenomenological fit parameters that probably represent mixes of microstructural features rather than unambiguous quantifications of specific tissue properties.”
§ NODDI in clinical research > 2.2. Is NODDI specific?
Load-bearingStrength:hedged· not yet calibratedTests✓ Asserted: passes? Checkable: unclear✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The debates on specificity and model validity have caused confusion among clinicians who are not familiar with the art of modeling and who wonder whether it is okay to use NODDI in their research.”
§ NODDI in clinical research > 2.2. Is NODDI specific?
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Important to note is that usual multi-shell dMRI data has limited information that allows estimation of only a handful of parameters.”
§ NODDI in clinical research > 2.2. Is NODDI specific?
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✗ Based: failsProbably not a substantial claim. The paper may give no reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“With regard to the degree of freedom, NODDI has 5 free parameters (NDI, ODI, f fw , and polar and azimuthal angles of the principal direction of the bundle), which is one less than DTI.”
§ NODDI in clinical research > 2.2. Is NODDI specific?
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The range of pathologies may be too diverse to be adequately captured with a single model, and models need to be validated in the target disease, not only in the healthy state.”
§ NODDI in clinical research > 2.2. Is NODDI specific?
Tests✓ Asserted: passes✗ Checkable: fails✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may be too vague to check against evidence. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Remember, apparent diffusion coefficient, virtually the only dMRI metric that has gained a presence in clinical practice, is a mix of a multitude of microstructural effects.”
§ NODDI in clinical research > 2.2. Is NODDI specific?
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Besides, the relationships between the model parameters and pathologies (e.g., atrophy and loss of axons, demyelination, microglial activation) are not one-to-one, and in reality different pathologies tend to coexist rather than occur in isolation.”
§ NODDI in clinical research > 2.2. Is NODDI specific?
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✗ Based: failsProbably not a substantial claim. The paper may give no reason why it holds. It may state two separate claims as one.
In the paper
“In a study of mild cognitive impairment, the mild cognitive impairment group had relatively greater ODI and smaller NDI than controls, although DTI was more sensitive to the group differences (Q.Wen et al., 2019b).”
§ NODDI in clinical research > 3.1. Alzheimer's disease
What the sources say
- Not matchedcites Q.Wen et al., 2019b
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Not matched
In the paper
“Another study, which compared healthy controls, subjects with mild cognitive impairment, and patients with Alzheimer's disease, reported that NDI was the most sensitive to group differences, and that NDI, ODI, and f fw were all correlated with cognitive score (Fu et al., 2019).”
§ NODDI in clinical research > 3.1. Alzheimer's disease
What the sources say
- Not matchedcites Fu et al., 2019
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Not matched
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“We also emphasize dependence on assumptions applies to all of the proposed biophysical models and does not necessarily undermine the value of NODDI.”
§ NODDI in clinical research > 2.2. Is NODDI specific?
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“The most widespread and successful clinical application of dMRI to date is the detection of acute ischemic infarction (Moseley et al., 1990).”
§ NODDI in clinical research > 3.6. Ischemia
What the sources say
- Not checked — no full text of the sourcecites Moseley et al., 1990 source
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“In addition, this work found a weak negative correlation between NDI and dendritic markers, which is counter-intuitive to the name 'neurite density index'.”
§ NODDI in clinical research > 3.3. Multiple sclerosis
What the sources say
- Not checked — no full text of the sourcecites Crombe et al., 2018 source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“Yet, there is an argument that those FCDs presented in (Winston et al., 2014) and (Rostampour et al., 2018) are readily detectable on conventional T1-/T2-weighted images (Chougar et al., 2018).”
§ NODDI in clinical research > 3.5. Epilepsy
What the sources say
- Not checked — no full text of the sourcecites Chougar et al., 2018 source
Strength:hedged· not yet calibratedTests✗ Asserted: fails✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The authors may not put it forward as true. The paper’s conclusions may not depend on it.
In the paper
“In addition, iNPH is primarily a disorder of cerebrospinal fluid dynamics that leads to cerebral dyshomeostasis, hypoperfusion, and hypometabolism (Bräutigam et al., 2019)”
§ NODDI in clinical research > 3.9. Idiopathic normal pressure hydrocephalus
What the sources say
- Not checked — no full text of the sourcecites Bräutigam et al., 2019 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“volume reduction and abnormal activation of the left superior temporal gyrus are reported to be associated with auditory hallucination in schizophrenia (Allen et al., 2007).”
§ NODDI in clinical research > 3.10. Schizophrenia
What the sources say
- Not checked — no full text of the sourcecites Allen et al., 2007 source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“A longitudinal study in athletes with concussion (Churchill et al., 2019) showed reduced NDI in WM in the early symptomatic phase of injury, and this decrease persisted at the time of return-to-play.”
§ NODDI in clinical research > 3.7. Traumatic brain injury
What the sources say
- Not checked — no full text of the sourcecites Churchill et al., 2019 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“In addition, increased ODI as well as decreased FA were also observed at both the early symptomatic phase and return-to-play.”
§ NODDI in clinical research > 3.7. Traumatic brain injury
What the sources say
- Not checked — no full text of the sourcecites Churchill et al., 2019 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Overall, despite the issue of the validity of the model assumptions, especially in the acute phase, NODDI has shown the ability to track brain alterations caused by ischemia and it may be a potentially useful means of predicting chronic disabilities.”
§ NODDI in clinical research > 3.6. Ischemia
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“In schizophrenia, a severe mental illness characterized by positive (e.g., hallucinations and delusions) and negative (e.g., anhedonia and flat affect) symptoms, axon disruption with concurrent reduced myelin levels and oligodendrocyte abnormalities has been postulated as a key pathology based on both imaging and postmortem studies (Davis et al., 2003;Vikhreva et al., 2016).”
§ NODDI in clinical research > 3.10. Schizophrenia
What the sources say
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Overall, the reported results and hypothetical interpretations of NODDI in TBI indicate the need to account for variabilities in time after injury, injury biomechanics, and individual pre-injury baseline.”
§ NODDI in clinical research > 3.7. Traumatic brain injury
Load-bearingStrength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
In the paper
“Some damaged axons show recovery with remyelination, whereas others progress into the irreversible stage characterized by axonal fragmentation and disconnection.”
§ NODDI in clinical research > 3.7. Traumatic brain injury
What the sources say
- Not checked — no full text of the sourcecites Armstrong et al., 2016 source
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“therefore, neurodegeneration is thought to be a consequence rather than a pathogenetic factor, and it remains uncertain as to what degree neurodegeneration explains the symptoms.”
§ NODDI in clinical research > 3.9. Idiopathic normal pressure hydrocephalus
What the sources say
- Not checked — no full text of the sourcecites Bräutigam et al., 2019 source
Strength:hedged· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“In a longitudinal follow-up, NDI recovered to values comparable with the non-compressed level at 6 months after surgery, with concurrent recovery of neurological score (Iwama et al., 2020).”
§ NODDI in clinical research > 3.12. Spondylotic myelopathy
What the sources say
- Not checked — no full text of the sourcecites Iwama et al., 2020 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“with gliomas and metastases tending to exhibit a higher extra-neurite fraction and a higher f fw , respectively (Fig. 8).”
§ NODDI in clinical research > 3.11. Brain tumors
What the sources say
- Not checked — no full text of the sourcecites Caverzasi et al., 2016 source
- Not matchedcites Kadota et al., 2018
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“NODDI has also revealed a regional variation in WM maturation, which is consistent with the known asynchrony of myelination and fiber development; maturation generally proceeds from posterior to anterior, and primary motor and sensory regions develop earlier than areas of higher order functions (Brody et al., 1987;Yakolev and Lecours, 1967).”
§ NODDI in clinical research > 4.2. Normal development and aging: perinatal to childhood
What the sources say
- Not checked — no full text of the sourcecites Brody et al., 1987 source
- Not matchedcites Yakolev and Lecours, 1967
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Strength:boosted· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Application of NODDI in clinical research has mostly reported promising results that dMRI biophysical models can be potentially useful for improving patient stratification and prediction of neurological functions.”
§ NODDI in clinical research > 5.1. Summary of clinical studies
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“In addition, the clinical value of NODDI needs to be evaluated in comparison with more accessible measures other than dMRI, with critical consideration given to cost effectiveness (Rao and Levin, 2012).”
§ NODDI in clinical research > 5.2. Toward a clinical tool
What the sources say
- Not checked — no full text of the sourcecites Rao and Levin, 2012 source
Strength:plain· not yet calibratedTests✓ Asserted: passes✗ Checkable: fails✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. It may be too vague to check against evidence. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Although NODDI is a simplified model, it is already complex compared with the current clinical standard, apparent diffusion coefficient which is simply the average of diffusivities measured along three orthogonal axes.”
§ NODDI in clinical research > 5.2. Toward a clinical tool
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In the vast majority of studies, disease-related effects were in directions that are biologically plausible, although this does not assure specificity to the tissue pathology.”
§ NODDI in clinical research > 5.1. Summary of clinical studies
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“After all, even if the model was correct, assigning a certain cellular structure to a certain compartment is somewhat ambiguous.”
§ NODDI in clinical research > 5.1. Summary of clinical studies
Strength:plain· not yet calibratedTests✓ Asserted: passes✗ Checkable: fails✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. It may be too vague to check against evidence. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Because dMRI parameters are indirect measures of tissue features and the underlying microstructure can only be speculated, hard-thinking about possible confounding effects is always required to interpret model parameters.”
§ NODDI in clinical research > 5.1. Summary of clinical studies
Strength:boosted· not yet calibratedTests✓ Asserted: passes✗ Checkable: fails✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. It may be too vague to check against evidence. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“Recently, impaired recognition of facial emotion expression in persons with autism spectrum disorder was reported to be linked with reduced NDI and ODI in the corpus callosum and cortical regions associated with viewing of a human face (Yasuno et al., 2020).”
§ NODDI in clinical research > 4.3. Developmental abnormalities
What the sources say
- Not checked — no full text of the sourcecites Yasuno et al., 2020 source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“It is important to note, however, that even if an imaging tool does not pass all the criteria to become part of clinical routine, the evidence accumulated during technical and biological/clinical validation can still show the usefulness of the tool in the basic research setting.”
§ NODDI in clinical research > 5.2. Toward a clinical tool
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Therefore, NODDI needs to be compared with the representations that suffice to explain the data, such as DKI.”
§ NODDI in clinical research > 5.2. Toward a clinical tool
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✗ Checkable: fails✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may be too vague to check against evidence.
In the paper
“In GM, (Eaton-Rosen et al., 2015) compared two time-points in infants born preterm (soon after birth and at term-equivalent age) and observed an increase of ODI in the cortex and an increase of NDI in the thalamus during the two time-points.”
§ NODDI in clinical research > 4.2. Normal development and aging: perinatal to childhood
What the sources say
- Not checked — no full text of the sourcecites Eaton-Rosen et al., 2015 source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“Recently, using an animal model and computer simulation, (Yi et al., 2019) showed that ODI may be sensitive to microglial density (due to increased occupancy in the extra-neurite space) and therefore could be a potential marker of neuroinflammation.”
§ NODDI in clinical research > 5.3. Specificity beyond NODDI
What the sources say
- Not matchedcites Yi et al., 2019
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Not matched
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“NODDI was originally developed for examining the adult brain and evidence is scarce on its applicability in infants and younger children.”
§ NODDI in clinical research > 4.2. Normal development and aging: perinatal to childhood
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“One possible explanation for the slow dissemination is that the diagnostic power of microstructure imaging does not yet have enough accumulated evidence to convince clinicians of its value.”
§ NODDI in clinical research > 5.2. Toward a clinical tool
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✗ Checkable: fails✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. It may be too vague to check against evidence. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“At present, we are not sure what biophysical phenomena have dominant effects on the dMRI signal, especially in disease states.”
§ NODDI in clinical research > 5.3. Specificity beyond NODDI
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✗ Based: failsProbably not a substantial claim. The paper may give no reason why it holds.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Difficulty in translation to actual clinical practice is not unique to dMRI; it is a universal issue for all kinds of biomarkers (Poste, 2011;Sung et al., 2003).”
§ NODDI in clinical research > 5.2. Toward a clinical tool
What the sources say
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“For example, aging is associated with axonal degeneration characterized by accumulation of organelles and increase of neurofilaments in axoplasm, myelin splitting and degeneration, increase of cellular debris, and proliferation and activation of glial cells (Peters, 2003).”
§ NODDI in clinical research > 5.3. Specificity beyond NODDI
What the sources say
- Not checked — no full text of the sourcecites Peters, 2003 source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“As a first-generation biophysical model designed for use in clinical settings, NODDI has achieved great success, as demonstrated by studies reporting sensitivity to disease-related effects and biologically plausible interpretations of the dMRI data.”
§ NODDI in clinical research > 5.5. Concluding remarks
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✗ Based: failsProbably not a substantial claim. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These processes are thought to result in increased hindrance of diffusion in both intra-and extra-axonal spaces.”
§ NODDI in clinical research > 5.3. Specificity beyond NODDI
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Imaging sensitive to glial cells could be of large clinical importance in the future because glial cells are the targets of several emerging therapeutic strategies (Hirsch and Hunot, 2009;Wilbanks et al., 2019).”
§ NODDI in clinical research > 5.3. Specificity beyond NODDI
What the sources say
Strength:hedged· not yet calibratedTests✓ Asserted: passes✗ Checkable: fails✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. It may be too vague to check against evidence. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“It should be noted that intensive application of a tool in clinical studies is not enough for it to cross the translational gap, and proof of specificity, technical validation, and cost effectiveness are likely to become bottlenecks for the clinical application of NODDI.”
§ NODDI in clinical research > 5.2. Toward a clinical tool
Tests✓ Asserted: passes✗ Checkable: fails✓ Load-bearing: passes✗ Based: failsProbably not a substantial claim. It may be too vague to check against evidence. The paper may give no reason why it holds. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Although substantial work remains to be done, we believe that NODDI represents a significant step toward application of microstructure imaging in realworld clinical practice.”
§ NODDI in clinical research > 5.5. Concluding remarks
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✗ Checkable: fails✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may be too vague to check against evidence.
The authors state this as an assumption.
Diffusion within each NODDI compartment is well described by a Gaussian distribution.
“NODDI belongs to a family of models that assume diffusion within each compartment is well described by a Gaussian distribution (i.e., diffusion tensor ellipsoid).”
The authors state this as an assumption.
The intra-neurite compartment can be modeled as a collection of infinitely thin 'sticks' with negligible perpendicular diffusivity.
“The intra-neurite compartment represents axons, and possibly dendritic processes, that are often referred to together as neurites, and is modeled as a collection of infinitely thin 'sticks' (signal attenuation due to diffusion in the perpendicular direction is negligible, d 0 i, μm 2 /ms) (Kroenke et al., 2004).”
The authors state this as an assumption.
The free water compartment is represented by isotropic diffusion with diffusivity 3 μm²/ms.
“The free water compartment is represented by isotropic diffusion with the diffusivity = d 3 fw μm 2 /ms.”
The authors state this as an assumption.
The orientation distribution function is constrained to the Watson distribution.
“In NODDI, the orientation distribution function is constrained to the Watson distribution, an axially symmetric distribution characterized by a single parameter.”
The authors state this as an assumption.
The parallel diffusivity of intra- and extra-neurite compartments is fixed at 1.7 μm²/ms and equal (tortuosity model).
“In addition, for the sake of stable estimation, the following constraints are imposed: (i) = = d d 1.7 µm /ms i, e ) e, i e, (tortuosity model; (Szafer et al., 1995)).”
The paper relies on this without support.
Data acquisition with stronger diffusion weightings beyond the normal DTI regimen, with b-values up to 2000-3000 s/mm2, is feasible in clinical settings with modern scanners.
“However, with modern scanners, data acquisition with stronger diffusion weightings beyond the normal DTI regimen, with b-values up to 2000-3000 s/mm 2 , is now feasible in clinical settings and it is expected that these data will further improve our understanding of the brain and diseases.”
The paper relies on this without support.
Axonal injury is the primary neuropathology in TBI, and a proxy for axon density derived from dMRI is promising for detecting it.
“Although there is no established imaging tool capable of detecting the neuronal damage in TBI (Eierud et al., 2014), axonal injury is generally believed to be the primary neuropathology and so a proxy for axon density derived from dMRI is thought promising.”
The paper relies on this without support.
Pre-operative prediction of surgical outcome in cervical spondylotic myelopathy is difficult or almost impossible.
“In addition, pre-operative prediction of surgical outcome is difficult or almost impossible.”
Citations
Cites
Staging of brain pathology related to sporadic Parkinson’s disease
Braak, H., Tredici, K. D., Rüb, U., de Vos, R. A. I., Jansen Steur, E. N. H., & Braak, E. (2003) · Neurobiology of Aging · doi:10.1016/s0197-4580(02)00065-9 · Cited by 10,777 · cited 2×
“(Adapted and reproduced with permission from (Braak et al., 2003)).”
BackgroundEstimation of the Effective Self-Diffusion Tensor from the NMR Spin Echo
Basser, P. J., Mattiello, J., & Bihan, D. L. (1994) · Journal of Magnetic Resonance Series B · doi:10.1006/jmrb.1994.1037 · Cited by 3,656
Mechanisms underlying inflammation in neurodegeneration
Glass, C. K., Saijo, K., Winner, B., Marchetto, M. C., & Gage, F. H. (2010) · Cell · doi:10.1016/j.cell.2010.02.016 · Cited by 3,580
NODDI: Practical in vivo neurite orientation dispersion and density imaging of the human brain
Zhang, H., Schneider, T., Wheeler-Kingshott, C. A., & Alexander, D. C. (2012) · NeuroImage · doi:10.1016/j.neuroimage.2012.03.072 · Cited by 3,288 · cited 3×
“Recent years have seen a marked proliferation of biophysical models with the explicit aim of clinically feasible data acquisition (single-diffusion encoding, b-values up to 2000–3000 s/mm(2), diffusion time 20–100 ms) (Fieremans et al., 2011; Hansen et al., 2017; Kaden et al., 2016; Zhang et al., 2012).”
BackgroundJensen, J. H., Helpern, J. A., Ramani, A., Lu, H., & Kaczynski, K. (2005) · Magnetic Resonance in Medicine · doi:10.1002/mrm.20508 · Cited by 2,488 · cited 7×
“In this review, we discuss the rationale behind using NODDI in clinical research, explore and summarize the applications of NODDI in human studies, and discuss perspectives for future research. https://doi.org/10.1016/j.jneumeth.2020.108908 Received 16 March 2020; Received in revised form 8 August 2020; Accepted 9 Aug…”
MethodInfluentialRegional Development of the Brain in Early Life
(1968) · Archives of Disease in Childhood · doi:10.1136/adc.43.229.388 · Cited by 2,107 · cited 1×
“…in WM maturation, which is consistent with the known asynchrony of myelination and fiber development; maturation generally proceeds from posterior to anterior, and primary motor and sensory regions develop earlier than areas of higher order functions (Brody et al., 1987; Yakolev and Lecours, 1967).”
BackgroundMultimodal population brain imaging in the UK Biobank prospective epidemiological study
Miller, K. L., Alfaro-Almagro, F., Bangerter, N. K., Thomas, D. L., Yacoub, E., Xu, J., Bartsch, A. J., Jbabdi, S., Sotiropoulos, S. N., Andersson, J. L. R., et al. (2016) · Nature Neuroscience · doi:10.1038/nn.4393 · Cited by 2,020
Neuroinflammation in Parkinson’s disease: A target for neuroprotection?
Hirsch, E. C., & Hunot, S. (2009) · The Lancet Neurology · doi:10.1016/s1474-4422(09)70062-6 · Cited by 1,984
Cortical demyelination and diffuse white matter injury in multiple sclerosis
Kutzelnigg, A., Lucchinetti, C. F., Stadelmann, C., Brück, W., Rauschka, H., Bergmann, M., Schmidbauer, M., Parisi, J. E., & Lassmann, H. (2005) · Brain · doi:10.1093/brain/awh641 · Cited by 1,836 · cited 1×
“This is thought to be due, at least partly, to the limited sensitivity of conventional MRI to histologically confirmed pathology (Kutzelnigg et al., 2005; Weinstein et al., 2015).”
BackgroundBlümcke, I., Thom, M., Aronica, E., Armstrong, D. D., Vinters, H. V., Palmini, A., Jacques, T. S., AVANZINI, G., Barkovich, A. J., Battaglia, G. S., et al. (2010) · Epilepsia · doi:10.1111/j.1528-1167.2010.02777.x · Cited by 1,746 · cited 1×
“FCD is pathologically characterized by abnormal cortical lamination with/without (FCD type I/II) large bizarre neurons and balloon cells (Blümcke et al., 2011).”
Background
Flagged first, then by citations
18 of the 281 references couldn’t be matched to a known paper.
Cited by
Sorted by citations
Parlatini, V., Itahashi, T., Lee, Y., Liu, S., Nguyen, T. T., Aoki, Y. Y., Forkel, S. J., Catani, M., Rubia, K., Zhou, J. H., et al. (2023) · Molecular Psychiatry · doi:10.1038/s41380-023-02173-1 · Cited by 107
“Nevertheless, the association we observed between callosal FA and age, as well as fi ndings from previous structural MRI studies, should encourage the longitudinal investigation of differences in the developmental trajectories of the white and gray matter in ADHD.”
ResultDimitrova, R., Pietsch, M., Ciarrusta, J., Fitzgibbon, S. P., Williams, L. Z. J., Christiaens, D., Cordero‐Grande, L., Batallé, D., Makropoulos, A., Schuh, A., et al. (2021) · NeuroImage · doi:10.1016/j.neuroimage.2021.118488 · Cited by 97
Kraguljac, N. V., Guerreri, M., Strickland, M. J., & Zhang, H. G. (2022) · Biological Psychiatry Global Open Science · doi:10.1016/j.bpsgos.2021.12.012 · Cited by 76
“This interpretation of the voxelwise MRI signals confers the fundamental advantage over the standard DTI and the more recent diffusion kurtosis imaging (22).”
BackgroundMethodInfluentialWidespread white matter oedema in subacute COVID-19 patients with neurological symptoms
Rau, A., Schroeter, N., Blazhenets, G., Dreßing, A., Walter, L. I., Kellner, E., Bormann, T., Mast, H., Wagner, D., Urbach, H., et al. (2022) · Brain · doi:10.1093/brain/awac045 · Cited by 63
“Relying on maximum likelihood estimation, the neurite orientation dispersion and density imaging (NODDI) technique is themost established one.(12) However, the NODDI approach requires stabilization by hard a priori constraints and is hampered by computing times of several hours for one dataset.”
BackgroundMethodHosp, J. A., Reisert, M., Dreßing, A., Götz, V., Kellner, E., Mast, H., Arndt, S., Waller, C. F., Wagner, D., Rieg, S., et al. (2024) · Nature Communications · doi:10.1038/s41467-024-48651-0 · Cited by 60
Metadata
- Authors
- Kamiya, K., Hori, M., & Aoki, S.
- Affiliations
- Toho University (JP)
- Juntendo University (JP)
- Corresponding author
- Kamiya, Kouhei
- Venue
- Journal of Neuroscience Methods
- Publisher
- Elsevier BV
- Published
- 2020-12
- Volume
- 346
- Pages
- 108908
- ISSN
- 0165-0270 (ISSN-L)
- OpenAlex
- W3049304068
- Semantic Scholar
- 4423ed0011e278c09c71720daeabdd56c94e251e
- Cited by
- 283
- References
- 281
- Citations by year
- 2026: 40 · 2025: 67 · 2024: 73 · 2023: 49 · 2022: 35 · 2021: 18 · 2020: 1
- FWCI
- 11.65
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience Methods (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Funders
- Japan Agency for Medical Research and Development
- Japan Society for the Promotion of Science
- Topics
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Advanced Neuroimaging Techniques and Applications
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Advanced MRI Techniques and Applications
- Life Sciences › Neuroscience › Cognitive Neuroscience › Functional Brain Connectivity Studies
- Keywords
- NODDI, diffusion MRI, microstructure modeling, clinical application, diffusion tensor imaging, tissue microstructure, clinical translation
- MeSH terms
- Brain, Humans, Neurites, Diffusion Magnetic Resonance Imaging, Diffusion Tensor Imaging
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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