The DOI matches its Crossref record; 49 of the 49 references it cites were found in a registry or an index; 2 of the 52 sources its claims cite were checked for support.
Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease
Open accessAbstract
Neurofilament light chain (NfL) is a promising fluid biomarker of disease progression for various cerebral proteopathies. Here we leverage the unique characteristics of the Dominantly Inherited Alzheimer Network and ultrasensitive immunoassay technology to demonstrate that NfL levels in the cerebrospinal fluid (n = 187) and serum (n = 405) are correlated with one another and are elevated at the presymptomatic stages of familial Alzheimer's disease. Longitudinal, within-person analysis of serum NfL dynamics (n = 196) confirmed this elevation and further revealed that the rate of change of serum NfL could discriminate mutation carriers from non-mutation carriers almost a decade earlier than cross-sectional absolute NfL levels (that is, 16.2 versus 6.8 years before the estimated symptom onset). Serum NfL rate of change peaked in participants converting from the presymptomatic to the symptomatic stage and was associated with cortical thinning assessed by magnetic resonance imaging, but less so with amyloid-β deposition or glucose metabolism (assessed by positron emission tomography). Serum NfL was predictive for both the rate of cortical thinning and cognitive changes assessed by the Mini-Mental State Examination and Logical Memory test. Thus, NfL dynamics in serum predict disease progression and brain neurodegeneration at the early presymptomatic stages of familial Alzheimer's disease, which supports its potential utility as a clinically useful biomarker.
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24 Own result · 18 Not checked yet · 8 Own method · 8 Own interpretation · 2 No basis given · 1 Partly supported · accuracy not yet measured
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“NfL levels in the cerebrospinal fluid (n = 187) and serum (n = 405) are correlated with one another”
- Also stated in: § Abstract · boosted
“CSF and serum NfL levels were tightly associated”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Abstract
boostedcorrelationaln = 187- Asserted: passes — The authors put it forward as true.
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- Also stated in: § Abstract · boosted
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“serum NfL was also increased at −6.8 EYO”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Abstract
plaincorrelationaln = 243- Asserted: passes — The authors put it forward as true.
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In the paper
“significant (predictive) associations were found between serum NfL rate of change and cortical thinning as well as MMSE and Logical Memory test”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Abstract
plaincorrelationaln = 39- Asserted: passes — The authors put it forward as true.
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In the paper
“was also predicative for a decrease in MMSE and Logical Memory scores”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Abstract
plaincorrelational- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“baseline NfL was highly predictive of future annualized cortical thinning, for both presymptomatic and symptomatic mutation carriers, at subsequent visits”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Abstract
boostedcorrelational- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“No differences in CSF or serum NfL levels between the three familial Alzheimer’s disease mutations were found”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Abstract
plainn = 243- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — 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 there was a positive relationship between NfL rate of change and the rate of change in precuneus amyloid-β deposition (amyloid-β-PET), the association did not reach significance”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Abstract
plaincorrelational- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“No differences in NfL rate of change were found between mutations in APP, PSEN1, and PSEN2”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Abstract
plain- Asserted: passes — The authors put it forward as true.
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A result the paper reports from its own data — 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 first EYO point where this increase became significant was at − 16.2 years”
- Also stated in: § Abstract · plain
“the NfL annual rate of change can distinguish non-carriers and mutation carriers as early as 16 years before the estimated symptom onset”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Abstract
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Also stated in: § Abstract · plain
A result the paper reports from its own data — 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 NfL rates of change were significantly elevated in mutation carriers relative to non-carriers”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Abstract
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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- Probably not a substantial claim. 18
- It may state two separate claims as one. 22
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“NfL is a component of the axonal cytoskeleton and is primarily expressed in large-caliber myelinated axons11,12.”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Abstract
What the sources say
- Partly supportedcites [11] Petzold, A. Neurofilament phosphoforms: surrogate markers for axonal injury, degeneration and loss. J. Neurol. Sci. 233, 183–198 (2005). sourceExperimental — accuracy not yet measured
Section 2 identifies NfL as a subunit of neurofilaments, which it calls dominant proteins of the axonal cytoskeleton. The passages found do not say that NfL is primarily expressed in large-caliber myelinated axons; discussion of axonal caliber and myelination does not establish that distribution. No page numbers are available in our copy. (LLM, conf=0.86)
- Partly supportedcites [12] Schlaepfer, W. W. & Lynch, R. G. Immunofluorescence studies of neurofilaments in the rat and human peripheral and central nervous system. J. Cell Biol. 74, 241–250 (1977). sourceExperimental — accuracy not yet measured
The paper describes neurofilaments as a major structural component of large axons and reports that they are particularly concentrated in large myelinated axons (pp. 241, 247). It also identifies a 68,000-dalton neurofilament-associated polypeptide, but does not explicitly identify it as NfL or establish that NfL specifically is primarily expressed in those axons. (LLM, conf=0.82)
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Partly supported
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“NfL rates of change in serum and rates of precuneus cortical thinning were significantly associated in symptomatic mutation carriers with a trend toward significance in presymptomatic mutation carriers”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Abstract
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — 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 rate of change in serum NfL peaked in the converter group with no further increase in the symptomatic carriers”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Abstract
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — 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 rate of change in serum NfL and the rate of change in precuneus glucose metabolism (18F-fluorodeoxyglucose (18F-FDG) PET) were significantly associated in symptomatic mutation carriers but not in presymptomatic mutation carriers”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Abstract
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“With this model the first bifurcation point was found at −18.6 years before EYO, the second at −5.8 years before EYO.”
- Also stated in: § Extended Data · plain
“A regression analysis was performed with two breaks of slope (see Methods for calculation).”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Extended Data
plainn = 196- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
- Also stated in: § Extended Data · plain
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 results indicate that NfL changes in the blood most closely reflect cortical thinning and support the view that serum NfL is primarily a marker of neurodegeneration.”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Abstract
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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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
“Advancements in NfL measurements have revealed tight correlations between NfL in the CSF and blood”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Abstract
boostedcorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
None of the sources cited for this claim have been checked yet.
In the paper
“Since the precuneus region has been shown to be most sensitive to Alzheimer’s disease pathophysiology in autosomal-dominant Alzheimer’s disease2,24, we focused our analyses on this region a priori.”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Methods > Imaging.
What the sources say
- Not checked yetcites [2] Gordon, B. A. et al. Spatial patterns of neuroimaging biomarker change in individuals from families with autosomal dominant Alzheimer’s disease: a longitudinal study. Lancet Neurol. 17, 241–250 (2018). source
- Not checked yetcites [24] Benzinger, T. L. S. et al. Regional variability of imaging biomarkers in autosomal dominant Alzheimer’s disease. Proc. Natl Acad. Sci. USA 110, E4502–E4509 (2013). source
boosted- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
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
“This suggests that longitudinal measures of NfL in the serum are a reliable, relatively cheap, and fast readout of neurodegeneration in the brain with comparable diagnostic value to neuroimaging but without the regional resolution.”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Abstract
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Collecting CSF requires an invasive procedure, and imaging is costly, so neither fits easily into routine care.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Clinical evaluators were blinded to each participant’s mutation status.”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Methods > Clinical assessment and EYO.
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“However, longitudinal analyses are largely missing and the importance of NfL as a molecular biomarker for the presymptomatic phase of neurodegenerative diseases remains unclear6,9,17.”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Abstract
What the sources say
- Not checked yetcites [6] Mattsson, N., Andreasson, U., Zetterberg, H. & Blennow, K. Association of plasma neurofilament light with neurodegeneration in patients with Alzheimer disease. JAMA Neurol. 74, 557–566 (2017). source
- Not checked yetcites [9] Weston, P. S. J. et al. Serum neurofilament light in familial Alzheimer disease: a marker of early neurodegeneration. Neurology 89, 2167–2175 (2017). source
- Not checked yetcites [17] Zhou, W. et al. Plasma neurofilament light chain levels in Alzheimer’s disease. Neurosci. Lett. 650, 60–64 (2017). source
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“For serum, the mean intra-assay coefficient of variation of duplicate determinations for concentration was 4.2%. In the CSF, the mean intra-assay coefficient of variation was 3.7%.”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Methods > NfL measurements in the CSF and blood.
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. 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
“In Alzheimer’s disease, presymptomatic changes in the brain include cortical thinning and neuropathological depositions containing amyloid-β and tau.”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Abstract
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Blood biomarkers for the presymptomatic phase of Alzheimer’s disease are largely lacking, although recent progress in the analysis of amyloid-β, tau, and neurofilament light chain (NfL) in the blood have been reported5–10.”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Abstract
What the sources say
- Not checked yetcites [5] Fandos, N. et al. Plasma amyloid β 42/40 ratios as biomarkers for amyloid β cerebral deposition in cognitively normal individuals. Alzheimers Dement. (Amst) 8, 179–187 (2017). source
- Not checked yetcites [6] Mattsson, N., Andreasson, U., Zetterberg, H. & Blennow, K. Association of plasma neurofilament light with neurodegeneration in patients with Alzheimer disease. JAMA Neurol. 74, 557–566 (2017). source
- Not checked yetcites [7] Nakamura, A. et al. High performance plasma amyloid-β biomarkers for Alzheimer’s disease. Nature 554, 249–254 (2018). source
- Not checked yetcites [8] Ovod, V. et al. Amyloid β concentrations and stable isotope labeling kinetics of human plasma specific to central nervous system amyloidosis. Alzheimers Dement. 13, 841–849 (2017). source
- Not checked yetcites [9] Weston, P. S. J. et al. Serum neurofilament light in familial Alzheimer disease: a marker of early neurodegeneration. Neurology 89, 2167–2175 (2017). source
- Not checked yetcites [10] Mielke, M. M. et al. Plasma phospho-tau181 increases with Alzheimer’s disease clinical severity and is associated with tau- and amyloid-positron emission tomography. Alzheimers Dement. 14, 989–997 (2018). source
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Changes of NfL in bodily fluids have been linked to brain damage and brain atrophy in mouse models and multiple neurological disorders including proteopathic neurodegenerative diseases11,13–16.”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Abstract
What the sources say
- Not checked yetcites [11] Petzold, A. Neurofilament phosphoforms: surrogate markers for axonal injury, degeneration and loss. J. Neurol. Sci. 233, 183–198 (2005). source
- Not checked yetcites [13] Bacioglu, M. et al. Neurofilament light chain in blood and CSF as marker of disease progression in mouse models and in neurodegenerative diseases. Neuron 91, 56–66 (2016). source
- Not checked yetcites [14] Barro, C. et al. Serum neurofilament as a predictor of disease worsening and brain and spinal cord atrophy in multiple sclerosis. Brain 141, 2382–2391 (2018). source
- Not checked yetcites [15] Brureau, A. et al. NF-L in cerebrospinal fluid and serum is a biomarker of neuronal damage in an inducible mouse model of neurodegeneration. Neurobiol. Dis. 104, 73–84 (2017). source
- Not checked yetcites [16] Kuhle, J. et al. Serum neurofilament light chain in early relapsing remitting MS is increased and correlates with CSF levels and with MRI measures of disease severity. Mult. Scler. 22, 1550–1559 (2016). source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
None of the sources cited for this claim have been checked yet.
In the paper
“The accumulation of amyloid-β in the brain (estimated 15–20 years before clinical onset) is followed by declines in cortical metabolism (estimated 10–15 years before clinical onset) and brain atrophy (5–10 years before clinical onset)1,2,22,25.”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Abstract
What the sources say
- Not checked yetcites [1] Bateman, R. J. et al. Clinical and biomarker changes in dominantly inherited Alzheimer’s disease. N. Engl. J. Med. 367, 795–804 (2012). source
- Not checked yetcites [2] Gordon, B. A. et al. Spatial patterns of neuroimaging biomarker change in individuals from families with autosomal dominant Alzheimer’s disease: a longitudinal study. Lancet Neurol. 17, 241–250 (2018). source
- Not checked yetcites [22] McDade, E. et al. Longitudinal cognitive and biomarker changes in dominantly inherited Alzheimer disease. Neurology 91, e1295–e1306 (2018). source
- Not checked yetcites [25] Burnham, S. C. et al. Clinical and cognitive trajectories in cognitively healthy elderly individuals with suspected non-Alzheimer’s disease pathophysiology (SNAP) or Alzheimer’s disease pathology: a longitudinal study. Lancet Neurol. 15, 1044–1053 (2016). source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. 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
“our observations suggest that this is the case in presymptomatic Alzheimer’s disease, while absolute NfL levels are better predictors in the symptomatic phase.”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Abstract
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Studies have indicated that the pathogenesis of familial and sporadic Alzheimer’s disease are very similar and share similar pathophysiology and progression36–39.”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Abstract
What the sources say
- Not checked yetcites [36] Bateman, R. J. et al. Autosomal-dominant Alzheimera’s disease: a review and proposal for the prevention of Alzheimera’s disease. Alzheimers Res. Ther. 3, 1 (2011). source
- Not checked yetcites [37] Cairns, N. J. et al. Neuropathologic assessment of participants in two multi-center longitudinal observational studies: the Alzheimer Disease Neuroimaging Initiative (ADNI) and the Dominantly Inherited Alzheimer Network (DIAN). Neuropathology 35, 390–400 (2015). source
- Not checked yetcites [38] Tang, M. et al. Neurological manifestations of autosomal dominant familial Alzheimer’s disease: a comparison of the published literature with the Dominantly Inherited Alzheimer Network observational study (DIAN-OBS). Lancet Neurol. 15, 1317–1325 (2016). source
- Not checked yetcites [39] Thomas, J. B. et al. Functional connectivity in autosomal dominant and late-onset Alzheimer disease. JAMA Neurol. 71, 1111–1122 (2014). source
hedged- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Increased absolute NfL levels in the blood in the symptomatic disease phase is consistent with similar observations in progressive supranuclear palsy28, Huntington’s disease30, and multiple sclerosis14.”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Abstract
What the sources say
- Not checked yetcites [28] Rojas, J. C. et al. Plasma neurofilament light chain predicts progression in progressive supranuclear palsy. Ann. Clin. Transl. Neurol. 3, 216–225 (2016). source
- Not checked yetcites [30] Byrne, L. M. et al. Neurofilament light protein in blood as a potential biomarker of neurodegeneration in Huntington’s disease: a retrospective cohort analysis. Lancet Neurol. 16, 601–609 (2017). source
- Not checked yetcites [14] Barro, C. et al. Serum neurofilament as a predictor of disease worsening and brain and spinal cord atrophy in multiple sclerosis. Brain 141, 2382–2391 (2018). source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“All samples were measured blinded.”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Methods > NfL measurements in the CSF and blood.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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 strong association between NfL levels in the CSF and blood indicates that NfL changes in the blood reflect changes in the brain”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Abstract
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The ADNI Imaging Core verified that the PET images were acquired using the established protocol and free of substantial artifacts.”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Methods > Imaging.
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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 association between NfL and cortical thinning, rather than amyloid-β deposition, is in line with cerebral amyloid-β aggregation being a trigger of subsequent neurodegeneration that, however, become independent of each other at later disease stages31.”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Abstract
What the sources say
- Not checked yetcites [31] Karran, E., Mercken, M. & De Strooper, B. The amyloid cascade hypothesis for Alzheimer’s disease: an appraisal for the development of therapeutics. Nat. Rev. Drug Discov. 10, 698–712 (2011). source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The ADNI Imaging Core screened images for artifacts and protocol compliance.”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Methods > Imaging.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“In the DIAN cohort, the increase of tau in the CSF (absolute levels, cross-sectional) occurs as early as 15 years before the estimated age of symptom onset32, which is much earlier than the increase of base-line NfL in the CSF.”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Abstract
What the sources say
- Not checked yetcites [32] Fagan, A. M. et al. Longitudinal change in CSF biomarkers in autosomal-dominant Alzheimer’s disease. Sci. Transl. Med. 6, 226ra230 (2014). source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Thus, CSF samples had one additional freeze–thaw cycle in Munich; however, prior work has indicated no significant effect of up to four freeze–thaw cycles on NfL in CSF43.”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Methods > NfL measurements in the CSF and blood.
What the sources say
- Not checked yetcites [43] Kuhle, J. et al. A comparative study of CSF neurofilament light and heavy chain protein in MS. Mult. Scler. 19, 1597–1603 (2013). source
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“These pathological changes can be assessed by magnetic resonance imaging (MRI), positron-emission tomography (PET), and measurement of amyloid-β and tau protein levels in the cerebrospinal fluid (CSF)1–4.”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Abstract
What the sources say
- Not checked yetcites [1] Bateman, R. J. et al. Clinical and biomarker changes in dominantly inherited Alzheimer’s disease. N. Engl. J. Med. 367, 795–804 (2012). source
- Not checked yetcites [2] Gordon, B. A. et al. Spatial patterns of neuroimaging biomarker change in individuals from families with autosomal dominant Alzheimer’s disease: a longitudinal study. Lancet Neurol. 17, 241–250 (2018). source
- Not checked yetcites [3] Jack, C. R. Jr. et al. NIA-AA Research Framework: toward a biological definition of Alzheimer’s disease. Alzheimers Dement. 14, 535–562 (2018). source
- Not checked yetcites [4] Sperling, R. A., Karlawish, J. & Johnson, K. A. Preclinical Alzheimer disease: the challenges ahead. Nat. Rev. Neurol. 9, 54–58 (2013). source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. 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
“In symptomatic Alzheimer’s disease, our results suggest that the NfL rate of change reaches a plateau, whereas absolute NfL levels continue to increase.”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Abstract
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Since the age of symptom onset tends to be consistent for a given mutation, it is possible to calculate for participants an estimated years to symptom onset (EYO) from the known onset of individuals with the same mutation20.”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Abstract
What the sources say
- Not checked yetcites [20] Ryman, D. C. et al. Symptom onset in autosomal dominant Alzheimer disease: a systematic review and meta-analysis. Neurology 83, 253–260 (2014). source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Note that the concentrations (pg ml−1) are calculated from the full-length NfL calibrator and thus may overestimate the concentration of an NfL fragment in the blood.”
§ Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease > Methods > NfL measurements in the CSF and blood.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper relies on this without support.
Collecting CSF requires an invasive procedure, and imaging is costly, so neither fits easily into routine care.
“However, CSF collection is invasive and imaging modalities are expensive; therefore, they are not well suited to routine clinical practice.”
The paper relies on this without support.
People with sporadic Alzheimer’s disease tend to be older and have more other illnesses, which could affect their blood NfL.
“However, sporadic Alzheimer’s disease patients are typically older and have more comorbidities, which in turn may influence NfL levels in the blood.”
The paper relies on this without support.
Rising NfL is not a signature of Alzheimer’s disease alone.
“While an increase of NfL levels is not specific for Alzheimer’s disease”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“The rates of disease progression, affected brain regions, and molecular cascades can vary significantly among individuals and across disease stages, posing significant challenges to the development of predictive models that accurately capture the dynamic pathology of AD417.”
From Artificial intelligence-driven multi-omics approaches in Alzheimer's disease: Progress, challenges, and future directions (2025) · cites this paper as [417]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“She also had relatively low plasma neurofilament light chain (NfL) measurements (20.24 pg/mL), a blood marker of axonal injury and neurodegeneration12 related to familial AD, particularly for her older age (her result and the mean and standard deviation of non-mutation carriers in the same age range, data not shown).”
From Resistance to autosomal dominant Alzheimer’s disease in an APOE3 Christchurch homozygote: a case report (2019) · cites this paper as [12]
Experimental — accuracy not yet measuredIn the citing paper
“We observed strong correlations between CSF and serum levels for NfL, as it has been previously reported [31, 88, 89].”
In the citing paper
“Studies of both ADAD and LOAD have demonstrated that rate of change in CSF and plasma NfL levels correlate with cortical thickness on structural MRI and cognitive performance”
From Alzheimer Disease: An Update on Pathobiology and Treatment Strategies (2019) · cites this paper as Preische et al., 2019
Statistics recomputed
Every reported test result, recomputed from its test statistic and degrees of freedom. A result shows as not adding up only once an independent check has confirmed it.
- ConsistentF(2, 104) = 1.8108reported p = .1686 · recomputed p = .169
“F(2, 104)= 1.8108, p = .1686”
- ConsistentF(2, 240) = 1.9205reported p = .1488 · recomputed p = .149
“F(2, 240)= 1.9205, p = .1488”
- ConsistentF(2, 130) = 0.4678reported p = .6274 · recomputed p = .627
“F(2, 130) = 0.4678, p = .6274”
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Self-check results appear here once an independent check has confirmed them.
Citations
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Metadata
- Authors
- Dominantly Inherited Alzheimer Network, Preische, O., Schultz, S. A., Apel, A., Kuhle, J., Kaeser, S. A., Barro, C., Gräber, S., Kuder-Buletta, E., LaFougere, C., Laske, C., Vöglein, J., Levin, J., Masters, C. L., Martins, R., Schofield, P. R., Rossor, M. N., Graff-Radford, N. R., Salloway, S., Ghetti, B., Ringman, J. M., Noble, J. M., Chhatwal, J., Goate, A. M., Benzinger, T. L. S., Morris, J. C., Bateman, R. J., Wang, G., Fagan, A. M., McDade, E. M., Gordon, B. A., & Jucker, M.
- Affiliations
- German Center for Neurodegenerative Diseases (DE)
- Washington University in St. Louis (US)
- University of Basel (CH)
- The University of Melbourne (AU)
- Edith Cowan University (AU)
- UNSW Sydney (AU)
- Mayo Clinic (US)
- Brown University (US)
- Keck Hospital of USC (US)
- Columbia University Irving Medical Center (US)
- Harvard University (US)
- Corresponding author
- Jucker, Mathias
- ORCID
- Schultz, Stephanie A.
- Kaeser, Stephan A.
- Barro, Christian
- Laske, Christoph
- Vöglein, Jonathan
- Levin, Johannes
- Masters, Colin L.
- Martins, Ralph
- Schofield, Peter R.
- Rossor, Martin N.
- Salloway, Stephen
- Ghetti, Bernardino
- Ringman, John M.
- Noble, James M.
- Chhatwal, Jasmeer
- Goate, Alison M.
- Benzinger, Tammie L. S.
- Morris, John C.
- Bateman, Randall J.
- Wang, Guoqiao
- Fagan, Anne M.
- McDade, Eric M.
- Gordon, Brian A.
- Jucker, Mathias
- Venue
- Nature Medicine
- Published
- 2019-01-21
- Volume
- 25
- Issue
- 2
- Pages
- 277-283
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- PMC
- PMC6367005
- OpenAlex
- W2910313823
- Cited by
- 927
- References
- 49
- Citations by year
- 2026: 70 · 2025: 87 · 2024: 145 · 2023: 116 · 2022: 126 · 2021: 142 · 2020: 176 · 2019: 63
- FWCI
- 87.98
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- UWA Profiles and Research Repository (UWA) (submittedVersion)
- Murdoch University Research Portal (submittedVersion)
- Edith Cowan University Research Online (Edith Cowan University) (submittedVersion)
- UCL Discovery (University College London) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- DZNE Pub (submittedVersion)
- Conicet (submittedVersion, cc-by)
- IUScholarWorks (Indiana University) (submittedVersion)
- PMC
- Funders
- National Institute for Health and Care Research (NF-SI-0512-10033)
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (320030)
- National Institutes of Health (UL1TR001873)
- Medical Research Council (MR/L023784/2, MR/L023784/1)
- Japan Society for the Promotion of Science (18K07385, 17H06498, 17K09794)
- National Institute on Aging (UF1AG032438, U19AG032438, U01AG032438, U24AG021886, K01AG053474)
- National Institute of Neurological Disorders and Stroke (P30NS098577)
- National Center for Advancing Translational Sciences
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Clinical Neurology › Amyotrophic Lateral Sclerosis Research
- Keywords
- neurofilament light chain, serum biomarkers, preclinical Alzheimer's disease, familial Alzheimer's disease, mutation carriers, disease progression, neurodegeneration, cortical thinning, amyloid-beta, glucose metabolism, cerebrospinal fluid, longitudinal biomarker dynamics, cognitive decline
- MeSH terms
- Alzheimer Disease, Humans, Mutation, Nerve Degeneration, Neurofilament Proteins, Disease Progression
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.
A language model drew the claims from the paper on 2026-10-01, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-01 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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