Cited by 33Dementia and Cognitive Impairment ResearchAlzheimer's disease research and treatmentsAdvanced MRI Techniques and Applications

T1rho MRI and CSF biomarkers in diagnosis of Alzheimer's disease

Open access
Haris, Mohammad, Yadav, Santosh K., Rizwan, Arshi, Singh, Anup, Cai, Kejia, Kaura, Deepak, Wang, Ena, Davatzikos, Christos +4 more·2015·NeuroImage: Clinical

Abstract

In the current study, we have evaluated the performance of magnetic resonance (MR) T1rho (T1ρ) imaging and CSF biomarkers (T-tau, P-tau and Aβ-42) in characterization of Alzheimer's disease (AD) patients from mild cognitive impairment (MCI) and control subjects. With informed consent, AD (n = 27), MCI (n = 17) and control (n = 17) subjects underwent a standardized clinical assessment and brain MRI on a 1.5-T clinical-scanner. T1ρ images were obtained at four different spin-lock pulse duration (10, 20, 30 and 40 ms). T1ρ maps were generated by pixel-wise fitting of signal intensity as a function of the spin-lock pulse duration. T1ρ values from gray matter (GM) and white matter (WM) of medial temporal lobe were calculated. The binary logistic regression using T1ρ and CSF biomarkers as variables was performed to classify each group. T1ρ was able to predict 77.3% controls and 40.0% MCI while CSF biomarkers predicted 81.8% controls and 46.7% MCI. T1ρ and CSF biomarkers in combination predicted 86.4% controls and 66.7% MCI. When comparing controls with AD, T1ρ predicted 68.2% controls and 73.9% AD, while CSF biomarkers predicted 77.3% controls and 78.3% for AD. Combination of T1ρ and CSF biomarkers improved the prediction rate to 81.8% for controls and 82.6% for AD. Similarly, on comparing MCI with AD, T1ρ predicted 35.3% MCI and 81.9% AD, whereas CSF biomarkers predicted 53.3% MCI and 83.0% AD. Collectively CSF biomarkers and T1ρ were able to predict 59.3% MCI and 84.6% AD. On receiver operating characteristic analysis T1ρ showed higher sensitivity while CSF biomarkers showed greater specificity in delineating MCI and AD from controls. No significant correlation between T1ρ and CSF biomarkers, between T1ρ and age, and between CSF biomarkers and age was observed. The combined use of T1ρ and CSF biomarkers have promise to improve the early and specific diagnosis of AD. Furthermore, disease progression form MCI to AD might be easily tracked using these two parameters in combination.

AI snapshot

Written from the paper’s full text.

TL;DR

This cross-sectional study compared T1ρ MRI of the medial temporal lobe with CSF biomarkers (T-tau, P-tau, Aβ1-42) for classifying AD, MCI, and control subjects. Combining T1ρ and CSF biomarkers improved prediction rates over either modality alone, especially for distinguishing AD from controls and MCI from controls.

Key findings

  • AD patients showed significantly higher GM T1ρ (p = 0.041), WM T1ρ (p = 0.005), T-tau (p = 0.001), and P-tau (p = 0.025), and significantly lower Aβ1-42 (p < 0.001) than controls. In MCI versus controls, only increased WM T1ρ reached significance (p = 0.05); in AD versus MCI, only T-tau was significantly increased (p = 0.05).
  • For controls vs AD, T1ρ predicted 68.2% of controls and 73.9% of AD; CSF biomarkers predicted 77.3% of controls and 78.3% of AD; the combination predicted 81.8% of controls and 82.6% of AD.
  • For MCI vs AD, T1ρ predicted 35.3% of MCI and 81.9% of AD; CSF biomarkers predicted 53.3% of MCI and 83.0% of AD; the combination predicted 57.3% of MCI and 84.6% of AD in the Results (the abstract states 59.3% MCI).
  • On ROC analysis, T1ρ had higher sensitivity and lower specificity than CSF biomarkers for MCI vs control (60% vs 53% sensitivity; 77% vs 82% specificity) and for AD vs control (82% vs 77% sensitivity; 71% vs 79% specificity). No significant correlations were observed between T1ρ and CSF biomarkers, T1ρ and age, or CSF biomarkers and age.

Methods

  • Cross-sectional study with 27 AD (mean age 76.8 ± 9.1 years), 17 MCI (71.93 ± 8.7 years), and 17 age-matched controls (70.2 ± 9.4 years); diagnoses used Petersen criteria for MCI and NINCDS–ADRDA criteria for probable AD.
  • Brain MRI was performed on a 1.5-T Siemens Sonata scanner. T1ρ images were acquired at spin-lock durations of 10, 20, 30, and 40 ms; T1ρ maps were generated by pixel-wise mono-exponential fitting, and T1ρ values were calculated from GM and WM of the left and right medial temporal lobe. CSF Aβ1-42, T-tau, and P-tau181p were measured using multiplex xMAP Luminex technology.
  • Analyses included Mann–Whitney U tests, binary logistic regression with enter method, ROC analysis, discriminant analysis for the three groups together, and Pearson correlations; p ≤ 0.05 was considered statistically significant.

Limitations

  • The paper states that the study is cross-sectional, comparing two diagnostic methods against clinical diagnosis as the gold standard, and that a longitudinal study with larger sample size is needed to assess these markers along the AD clinical continuum.
  • Evident from the text: sample sizes are small (27 AD, 17 MCI, 17 controls), MCI prediction was poor for T1ρ alone and modest even in combination, and the study used a single 1.5-T scanner without postmortem confirmation of pathology.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.1016/j.nicl.2015.02.016

Cites

53 of 53 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

13 of 28 cited sources checked · 4 supported · 1 flagged · accuracy not yet measured

  • Premisecitation

    A number of studies have suggested that CSF markers in combination with neuroimaging and neuropsychological tools add to the accuracy of AD diagnosis.

    “A number of studies have suggested that CSF markers in combination with neuroimaging and neuropsychological tools add to the accuracy of AD diagnosis (Richard et al., 2013; Schuff et al., 2009; Vemuri et al., 2010).”
    Quote in the paperSubstantial claim3 of 3 sources checked
    • cites Richard et al., 2013 source

      The Discussion (Implications for clinical practice and research; page not provided) concludes that neither MRI nor CSF analysis importantly increases diagnostic accuracy for progression to AD in patients with mild cognitive impairment when a brief memory test is administered first. That is contrary to attributing an accuracy gain from combining these tools to this study. (LLM, conf=0.88)

      Checked by a reasoning model — may be wrong.

      Experimental — accuracy not yet measured
    • cites Schuff et al., 2009 source

      The Introduction and Discussion describe using CSF markers with MRI and say the two measures provide complementary information about Alzheimer’s disease pathology. But the Discussion explicitly says their diagnostic value together remains unclear, and the paper does not show that adding neuropsychological tools improves diagnostic accuracy. Page numbers are unavailable in our copy. (LLM, conf=0.86)

      Experimental — accuracy not yet measured
    • cites Vemuri et al., 2010 source

      The discussion (pp. 143–151; passage does not identify a specific page) says MRI and CSF biomarkers are both needed to characterize different aspects of AD pathology, and the Methods describes cognitive assessments alongside both biomarkers. But the paper does not show that combining these tools improves the accuracy of AD diagnosis; its reported discrimination analyses assess changes in the biomarkers separately. (LLM, conf=0.84)

      Experimental — accuracy not yet measured
  • Premisecitation

    Elevated CSF T-tau level is not specific to AD as it may also be elevated in other neurodegenerative diseases.

    “However, clinical studies have shown that the elevated CSF T-tau level is not specific to AD as it may also be elevated in other neurodegenerative diseases (Arai et al., 1997; Urakami et al., 2001).”
    Quote in the paperNot a substantial claim1 of 2 sources checked
    • cites Arai et al., 1997 source
    • cites Urakami et al., 2001 source
  • Premisereasoning

    Watts et al. found ~7-10% lower T1ρ value both in GM and WM compared to the current study.

    “In addition, Watts et al. have found ~7–10% lower T1ρ value both in GM and WM compared to the current study.”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites Watts et al., 2014 source

      Table 1 (page not provided) reports mean T1ρ values for cortical GM and for juxtacortical WM and major WM tracts. The paper does not give the citing study’s values, so its text cannot establish that these measurements are approximately 7–10% lower. (LLM, conf=0.84)

      Experimental — accuracy not yet measured
  • Premisecitation

    With higher field strength T1ρ decreases.

    “and it is well known fact that with higher field strength T1ρ decreases (Singh et al., 2014).”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites Singh et al., 2014 source

      The Results section (‘T1ρ Analysis at 3T vs 7T’) reports significantly lower T1ρ values at 7T than at 3T in human knee cartilage (n = 6). That supports the direction of the comparison, but the paper does not establish an unqualified rule that T1ρ decreases with higher field strength across tissues or measurement conditions; the Discussion also notes that the spin-lock power used could have contributed to the lower values. (LLM, conf=0.86)

      Experimental — accuracy not yet measured
  • Findingown data

    When delineating AD from control, T1ρ showed 82% sensitivity and 71% specificity.

    “When delineating AD from control T1ρ showed 82% sensitivity and 71% specificity”
    Quote in the paperSubstantial claim
  • May combine two claims. 20
  • Classified as probably not a substantial claim. 16
  • May combine two claims.

    Premisecitation

    CSF measures of T-tau and Aβ1-42 levels are individually sensitive but have lower specificity for AD against other dementia disorders.

    “It has been found that the CSF measures of total tau (T-tau) and amyloid beta (Aβ1-42) levels are individually sensitive though but with lower specificity for AD against other dementia disorders (Blennow, 2004).”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites Blennow, 2004 source
  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Watts et al. observed a positive correlation between WM T1ρ and age while GM T1ρ showed negative correlation with age.

    “Recently, Watts et al., have evaluated the age dependence changes in GM and WM T1ρ relaxation times in brain of normal human volunteers on a 3-T MRI scanner (Watts et al., 2014). They have observed a positive correlation between WM T1ρ and age while the GM T1ρ showed negative correlation with age.”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites Watts et al., 2014 source
  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Medial temporal lobe atrophy on MRI is considered an early and sensitive marker for AD, and is assumed to reflect underlying neuronal loss in hippocampus and temporal lobe.

    “Medial temporal lobe (MTA) atrophy as observed on MRI is considered to be an early and sensitive marker for AD, and is assumed that it reflects underlying neuronal loss in hippocampus and temporal lobe (Clerx et al., 2013; Jack et al., 1997; Duara et al., 2008).”
    Quote in the paperNot a substantial claim3 of 3 sources checked
    • cites Clerx et al., 2013 source

      The Introduction describes MRI-assessed medial temporal lobe atrophy as an effective aid to early AD diagnosis, and §4.1.1 calls medial temporal neurodegeneration a strong MRI marker of imminent conversion. The paper does not state that the MRI finding reflects neuronal loss in the hippocampus and temporal lobe; §4.1.3 notes that some atrophy measures may reflect more generalized atrophy. (LLM, conf=0.84)

      Experimental — accuracy not yet measured
    • cites Jack et al., 1997 source

      The Abstract describes MRI-based hippocampal volume as a sensitive marker of medial temporal neuroanatomic degeneration early in AD, and the Discussion reports that it distinguishes very mild AD from elderly controls. The paper does not establish the more specific assumption that the MRI atrophy reflects neuronal loss in the hippocampus and temporal lobe. (LLM, conf=0.85)

      Experimental — accuracy not yet measured
    • cites Duara et al., 2008 source

      The Abstract reports that MRI-based MTA scores distinguish probable AD and amnestic MCI from comparison groups, with 85% sensitivity for probable AD at the reported cut score. The GLOSSARY discussion says MTA may serve as an early marker and correlates with medial temporal degenerative pathology at autopsy. It does not specifically identify neuronal loss in the hippocampus and temporal lobe as what the MRI finding reflects. Page numbers are not available for these passages. (LLM, conf=0.84)

      Experimental — accuracy not yet measured
  • Classified as probably not a substantial claim.

    Premisecitation

    Previous studies have shown higher T1ρ value in the medial temporal lobe of AD compared to those of MCI and control.

    “Previous studies have shown higher T1ρ value in the medial temporal lobe (MTL) of AD compared to those of mild cognitive impairment (MCI) and control (Haris et al., 2011; Borthakur et al., 2008).”
    Quote in the paperSubstantial claim1 of 2 sources checked
    • cites Haris et al., 2011 source
    • cites Borthakur et al., 2008 source
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    P-tau showed better specificity for AD compared with T-tau.

    “In a recent study, Hampel's group reported that when compared with T-tau, P-tau showed better specificity for AD (Hampel, and Blennow, 2004).”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites Hampel, and Blennow, 2004 source

      The “Phosphorylated tau protein” section says P-tau’s specificity for differentiating AD from other dementias seems higher than T-tau’s, and the P-tau181 subsection reports improved specificity for distinguishing AD from LBD. But the paper is a review, and its P-tau181 subsection also reports one comparison in which P-tau181 had 94% specificity versus 100% for T-tau. It therefore does not support an unqualified claim of better specificity across comparisons. (LLM, conf=0.86)

      Experimental — accuracy not yet measured
  • May combine two claims.

    Findingown data

    A negative correlation trend between Aβ1-42 and T1ρ was observed in controls and MCI subjects, while in AD patients this correlation showed a positive trend.

    “A negative correlation trend between Aβ1-42 and T1ρ was observed in controls and MCI subjects, while in AD patients this correlation showed a positive trend.”
    Quote in the paperNot a substantial claim
  • May combine two claims.

    Findingown data

    On ROC analysis, T1ρ showed greater sensitivity (60%) and less specificity (77%) than CSF biomarkers (53% and 82%) in discriminating MCI from control.

    “On ROC analysis, T1ρ showed greater sensitivity (60%) and less specificity (77%) than CSF biomarkers (53% and 82%) in discriminating MCI from control”
    Quote in the paperSubstantial claim
  • May combine two claims.

    Findingown data

    WM T1ρ in MCI subjects and both GM T1ρ and WM T1ρ in AD patients showed an increasing trend with age.

    “However, WM T1ρ in MCI subjects and both GM T1ρ and WM T1ρ in AD patients showed an increasing trend with age”
    Quote in the paperNot a substantial claim
  • May combine two claims.

    Findingown data

    When three groups were taken together, T1ρ and CSF biomarkers classified 54.5% of controls, 40% of MCI subjects, and 65.2% of AD patients.

    “When combined three groups together, T1ρ and CSF biomarkers were able to classify 54.5% controls, 40% MCI subjects and 65.2% AD patients.”
    Quote in the paperSubstantial claim
  • May combine two claims.

    Findingown data

    These two biomarkers misclassified 31.8% of controls as MCI subjects and 13.6% of controls as AD patients.

    “These two biomarkers misclassified 31.8% controls as MCI subjects and 13.6% controls as AD patients”
    Quote in the paperNot a substantial claim
  • May combine two claims.

    Findingown data

    In MCI subjects, T-tau and P-tau were higher and Aβ1-42 lower than in controls, but these differences were not statistically significant.

    “MCI subjects showed higher T1ρ, T-tau, P-tau and lower Aβ1-42 compared to control subjects. However, only increase in WM T1ρ (p = 0.05) reached to the statistical significant level”
    Quote in the paperNot a substantial claim
  • May combine two claims.

    Findingown data

    8.7% of AD patients were falsely predicted as controls and 26.1% of AD patients as MCI subjects.

    “There were false prediction of 8.7% AD patients as controls and 26.1% AD patients as MCI subjects.”
    Quote in the paperNot a substantial claim
  • May combine two claims.

    Findingown data

    33.3% of MCI subjects were falsely predicted as controls and 26.7% of MCI subjects as AD patients.

    “while 33.3% MCI subjects were falsely predicted as controls and 26.7% MCI subjects as AD patients.”
    Quote in the paperNot a substantial claim
  • May combine two claims.

    Interpretationown data

    MCI subjects showed significantly higher WM T1ρ compared to controls, which suggests that abnormality occurs earlier in WM than GM.

    “MCI subjects showed significantly higher WM T1ρ compared to controls, which suggests that abnormality occur earlier in WM than GM.”
    Quote in the paperSubstantial claim
  • May combine two claims.

    Interpretationown data

    Both CSF biomarkers and T1ρ MRI seem to have incremental value in diagnosis of AD.

    “In conclusion, both CSF biomarkers and T1ρ MRI seem to have incremental value in diagnosis of AD.”
    Quote in the paperSubstantial claim
  • Probably not a substantial claim: may not pass S4 (based).

    Premisenone given

    To date none of the MRI methods has proven to be an accurate in-vivo marker for early diagnosis of AD.

    “However, to date none of the MRI methods has proven to be an accurate in-vivo marker for early diagnosis of AD.”
    Quote in the paperNot a substantial claim
  • May combine two claims.

    Interpretationown data

    No correlation between T1ρ and CSF biomarkers suggests that these two biomarkers are independent to each other and have differential diagnostic efficacy.

    “In the current study, no correlation between T1ρ and CSF biomarkers suggests that these two biomarkers are independent to each other and have differential diagnostic efficacy.”
    Quote in the paperSubstantial claim
  • May combine two claims.

    Interpretationown data

    Significantly higher GM and WM T1ρ in AD compared to controls imply that in AD abnormality persists both in GM and WM.

    “Significantly higher GM and WM T1ρ in AD compared to controls imply that in AD abnormality persist both in GM and WM.”
    Quote in the paperSubstantial claim
  • May combine two claims.

    Interpretationown data

    No correlation between T1ρ and age suggests that the increased T1ρ is due to changes in underlying pathology instead of any age related changes.

    “No correlation between T1ρ and age was observed which suggests that the increased T1ρ is due to changes in underlying pathology instead of any age related changes.”
    Quote in the paperSubstantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    A standardized clinical assessment including medical history, physical and neurological examination, psychometric evaluation, and brain MRI was performed in all patients.

    “A standardized clinical assessment including medical history, physical and neurological examination, psychometric evaluation, and brain MRI was performed in all patients.”
    Quote in the paperNot a substantial claim
  • May combine two claims.

    Premisecitation

    Majority of studies have reported decreased Aβ1-42, and increased T-tau and P-tau levels in CSF of MCI and AD patients.

    “Majority of studies have reported decreased Aβ1-42, and increased T-tau and P-tau levels in CSF of MCI and AD patients (Hansson et al., 2006; Mattsson et al., 2009; Andreasen et al., 2001, 2003) and our findings are in conformity with those studies.”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites Hansson et al., 2006 source
    • cites Mattsson et al., 2009 source
    • cites Andreasen et al., 2001, 2003

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    Institutional Review Board of the University of Pennsylvania approved the current study protocol.

    “Institutional Review Board of the University of Pennsylvania approved the current study protocol.”
    Quote in the paperNot a substantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Some studies observed no relation between CSF tau or Aβ1-42 and whole-brain atrophy, while others found a significant inverse relationship between CSF P-tau and hippocampal volume in MCI.

    “Some observed no relation between CSF tau or Aβ1-42 and whole-brain atrophy (Sluimer et al., 2010), while others found a significant inverse relationship between CSF P-tau and hippocampal volume in MCI (Herukka et al., 2008).”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites Sluimer et al., 2010 source
    • cites Herukka et al., 2008 source
  • Classified as probably not a substantial claim.

    Study design and conductcitation

    Diagnoses of MCI were made according to the Petersen criteria for MCI.

    “Diagnoses of MCI was made according to the Petersen criteria for MCI (Petersen et al., 2001)”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites Petersen et al., 2001 source
  • Classified as probably not a substantial claim.

    Study design and conductcitation

    AD patients were diagnosed according to the NINCDS-ADRDA criteria for probable AD.

    “while the AD patients were diagnosed according to the National Institute of Neurological and Communicative Diseases and Stroke/Alzheimer's Disease and Related Disorders Association criteria (NINCDS–ADRDA) for probable AD (McKhann et al., 1984).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites McKhann et al., 1984 source
  • May combine two claims.

    Premisecitation

    MTA may also be present in other types of dementia and absence of MTA does not exclude the diagnosis of AD especially in the early stage.

    “However, MTA may also be present in other types of dementia (Tam et al., 2005; Barber et al., 1999) and absence of MTA does not exclude the diagnosis of AD especially in the early stage.”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites Tam et al., 2005 source
    • cites Barber et al., 1999 source
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisenone given

    T1ρ MRI has capability to probe the protein contents in various tissues such as brain, blood and cartilage.

    “T1ρ MRI has capability to probe the protein contents in various tissues such as brain, blood and cartilage.”
    Quote in the paperNot a substantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Borthakur et al. have shown the feasibility of T1ρ imaging in evaluating the plaques burden in a mouse model of AD.

    “Borthakur et al. have shown the feasibility of T1ρ imaging in evaluating the plaques burden in a mouse model of AD (Borthakur et al., 2006a).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Borthakur et al., 2006a

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • Classified as probably not a substantial claim. May combine two claims.

    Study design and conductnone given

    The control group consisted of patients who presented to the memory clinic with subjective complaints and underwent exactly the same diagnostic work-up as the MCI and AD patients.

    “The control group consisted of patients, who presented to our memory clinic with subjective complaints, and underwent exactly the same diagnostic work-up as the MCI and AD patients.”
    Quote in the paperSubstantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Increased CSF tau level corresponds to higher baseline hippocampal volume in AD.

    “It has been shown that the increased CSF tau level corresponds to the higher baseline hippocampal volume in AD.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Hampel et al., 2005 source
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    No significant effect of T-tau level on hippocampal atrophy was reported.

    “The same study has also reported, no significant effect of T-tau level on hippocampal atrophy (Hampel et al., 2005).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Hampel et al., 2005 source
  • Classified as probably not a substantial claim.

    Study design and conductnone given

    Diagnoses were made by a team consisting of neurologist, neuropsychologist, and psychiatrist who performed extensive behavioral, neuropsychological, and neuroimaging assessments.

    “Diagnoses was made by a team consisting of neurologist, neuropsychologist, and psychiatrist who performed extensive behavioral, neuropsychological, and neuroimaging assessments.”
    Quote in the paperSubstantial claim
32 of 32
  • The paper relies on this without support.

    Clinical diagnosis is the gold standard for classifying subjects as AD, MCI, or control.

    “the values of two different diagnostic methods were compared in subject with the clinical diagnosis as gold standard.”
  • The paper relies on this without support.

    Control subjects with subjective complaints but no diagnosis are representative of normal controls.

    “The control group consisted of patients, who presented to our memory clinic with subjective complaints, and underwent exactly the same diagnostic work-up as the MCI and AD patients.”
2 of 2

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • Reported control classifications cannot come from 17 controls

    Major

    The paper states that there were 17 controls, but the reported three-group classification percentages cannot represent whole numbers of 17 people: 31.8% and 13.6% correspond instead to 7 and 3 out of 22 controls. No different control-group size is stated for this analysis.

  • Combined MCI prediction rate differs between abstract and results

    Minor

    For the combined CSF biomarker and T1ρ analysis distinguishing MCI from AD, the abstract reports 59.3% of MCI subjects predicted, while the results report 57.3%.

  • Combined control prediction rate differs between results and discussion

    Minor

    The combined analysis distinguishing controls from AD reports 81.8% for controls in the results, but 81.2% in the discussion; both give 82.6% for AD.

3 of 3

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Authors
Haris, M., Yadav, S. K., Rizwan, A., Singh, A., Cai, K., Kaura, D., Wang, E., Davatzikos, C., Trojanowski, J. Q., Melhem, E. R., Marincola, F. M., & Borthakur, A.
Affiliations
  • Sidra Medical and Research Center (QA)
  • All India Institute of Medical Sciences (IN)
  • Indian Institute of Technology Delhi (IN)
  • University of Illinois Chicago (US)
  • University of Pennsylvania (US)
Corresponding author
Haris, Mohammad
Venue
NeuroImage: Clinical
Publisher
Elsevier BV
Published
2015
Volume
7
Pages
598-604
ISSN
2213-1582 (ISSN-L)
OpenAlex
W2070126554
Cited by
33
References
53
Citations by year
2025: 1 · 2024: 2 · 2023: 5 · 2022: 4 · 2021: 1 · 2020: 6 · 2019: 1 · 2018: 2 · 2017: 5 · 2016: 4 · 2015: 2
FWCI
3.52
Type
journal article
Language
en
Open access
Locations
  • NeuroImage Clinical (publishedVersion, cc-by-nc-nd)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
Funders
  • NIH (RR02305)
  • Pennsylvania State Tobacco Settlement (SAP4100027296)
Topics
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Advanced MRI Techniques and Applications
Keywords
Alzheimer's disease, mild cognitive impairment, T1rho MRI, cerebrospinal fluid biomarkers, tau protein, phosphorylated tau, amyloid-beta 42, medial temporal lobe, early diagnosis, diagnostic accuracy, sensitivity and specificity
MeSH terms
Aged, Alzheimer Disease, Female, Humans, Image Interpretation, Computer-Assisted, Magnetic Resonance Imaging, Male, Neuropsychological Tests, ROC Curve, Sensitivity and Specificity, Biomarkers, Amyloid beta-Peptides, tau Proteins, Area Under Curve, Cognitive Dysfunction

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