Evidence map›Paper›PMID 28158844›Full record

ArticleJournal of neuropathology and experimental neurology2017

Association of Neuropathological Markers in the Parietal Cortex With Antemortem Cognitive Function in Persons With Mild Cognitive Impairment and Alzheimer Disease.

Cyntia Tremblay, Arnaud François, Charlotte Delay, Laure Freland, Milène Vandal, David A Bennett, Frédéric Calon

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neuropathology and experimental neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. A Meta-Analysis on Presynaptic Changes in Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2024
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Lower GLUT1 and unchanged MCT1 in Alzheimer's disease cerebrovasculature.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 3 countries.

Cyntia TremblayFrom the Faculté de pharmacie, Université Laval, Québec, QC, Canada (CT, AF, LF, MV, FC); Centre Hospitalier Universitaire de Québec (CHU-Q) Research Center, Neuroscience Axis, Québec, QC, Canada (CT, AF, LF, MV, FC); "Facteurs de risque et déterminants moléculaires des maladies liées au vieillissement" (RID-AGE) Research Group, University of Lille, INSERM U1167, Lille University Medical Center, Institut Pasteur de Lille, Lille, France (CD); and Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL (DAB).
Arnaud FrançoisFrom the Faculté de pharmacie, Université Laval, Québec, QC, Canada (CT, AF, LF, MV, FC); Centre Hospitalier Universitaire de Québec (CHU-Q) Research Center, Neuroscience Axis, Québec, QC, Canada (CT, AF, LF, MV, FC); "Facteurs de risque et déterminants moléculaires des maladies liées au vieillissement" (RID-AGE) Research Group, University of Lille, INSERM U1167, Lille University Medical Center, Institut Pasteur de Lille, Lille, France (CD); and Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL (DAB).
Charlotte DelayFrom the Faculté de pharmacie, Université Laval, Québec, QC, Canada (CT, AF, LF, MV, FC); Centre Hospitalier Universitaire de Québec (CHU-Q) Research Center, Neuroscience Axis, Québec, QC, Canada (CT, AF, LF, MV, FC); "Facteurs de risque et déterminants moléculaires des maladies liées au vieillissement" (RID-AGE) Research Group, University of Lille, INSERM U1167, Lille University Medical Center, Institut Pasteur de Lille, Lille, France (CD); and Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL (DAB).
Laure FrelandFrom the Faculté de pharmacie, Université Laval, Québec, QC, Canada (CT, AF, LF, MV, FC); Centre Hospitalier Universitaire de Québec (CHU-Q) Research Center, Neuroscience Axis, Québec, QC, Canada (CT, AF, LF, MV, FC); "Facteurs de risque et déterminants moléculaires des maladies liées au vieillissement" (RID-AGE) Research Group, University of Lille, INSERM U1167, Lille University Medical Center, Institut Pasteur de Lille, Lille, France (CD); and Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL (DAB).
Milène VandalFrom the Faculté de pharmacie, Université Laval, Québec, QC, Canada (CT, AF, LF, MV, FC); Centre Hospitalier Universitaire de Québec (CHU-Q) Research Center, Neuroscience Axis, Québec, QC, Canada (CT, AF, LF, MV, FC); "Facteurs de risque et déterminants moléculaires des maladies liées au vieillissement" (RID-AGE) Research Group, University of Lille, INSERM U1167, Lille University Medical Center, Institut Pasteur de Lille, Lille, France (CD); and Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL (DAB).
David A BennettFrom the Faculté de pharmacie, Université Laval, Québec, QC, Canada (CT, AF, LF, MV, FC); Centre Hospitalier Universitaire de Québec (CHU-Q) Research Center, Neuroscience Axis, Québec, QC, Canada (CT, AF, LF, MV, FC); "Facteurs de risque et déterminants moléculaires des maladies liées au vieillissement" (RID-AGE) Research Group, University of Lille, INSERM U1167, Lille University Medical Center, Institut Pasteur de Lille, Lille, France (CD); and Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL (DAB).
Frédéric CalonFrom the Faculté de pharmacie, Université Laval, Québec, QC, Canada (CT, AF, LF, MV, FC); Centre Hospitalier Universitaire de Québec (CHU-Q) Research Center, Neuroscience Axis, Québec, QC, Canada (CT, AF, LF, MV, FC); "Facteurs de risque et déterminants moléculaires des maladies liées au vieillissement" (RID-AGE) Research Group, University of Lille, INSERM U1167, Lille University Medical Center, Institut Pasteur de Lille, Lille, France (CD); and Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL (DAB).
Université Laval · CACentre hospitalier universitaire de Québec · CAInstitut Pasteur de Lille · FRRush University Medical Center · US

Funding

SUPPLEMENT TO RUSH ALZHEIMERS DISEASE CENTER COREP30AG010161 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BENNETT, DAVID ALAN · 1991 to 2020
$49.1M
RISK FACTORS, PATHOLOGY, AND CLINICAL EXPRESSIONS OF ADR01AG015819 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BENNETT, DAVID ALAN · 1998 to 2024
$21.4M
Risk Factors, Pathology, and Clinical Expressions of ADRF1AG015819 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BENNETT, DAVID ALAN · 2014 to 2014
$6.0M
NIA NIH HHS P30 AG010161NIA NIH HHS R01 AG015819NIA NIH HHS RF1 AG015819
6 · The paper itself

Abstract

The associations between cognitive function and neuropathological markers in patients with mild cognitive impairment (MCI) and Alzheimer disease (AD) remain only partly defined. We investigated relationships between antemortem global cognitive scores and β-amyloid (Aβ), tau, TDP-43, synaptic proteins and other key AD neuropathological markers assessed by biochemical approaches in postmortem anterior parietal cortex samples from 36 subjects (12 MCI, 12 AD and 12 not cognitively impaired) from the Religious Orders Study. Overall, the strongest negative correlation coefficients associated with global cognitive scores were obtained for insoluble phosphorylated tau (r2 = -0.484), insoluble Aβ42 (r2 = -0.389) and neurofibrillary tangle counts (r2 = -0.494) (all p < 0.001). Robust inverse associations with cognition scores were also established for TDP-43-positive cytoplasmic inclusions (r2 = -0.476), total insoluble tau (r2 = -0.385) and Aβ plaque counts (r2 = -0.426). Sarkosyl (SK)- or formic acid (FA)-extracted tau showed similar interrelations. On the other hand, synaptophysin (r2 = +0.335), pS403/404 TDP-43 (r2 = +0.265) and septin-3 (r2 = +0.257) proteins positively correlated with cognitive scores. This study suggests that tau and Aβ42 in their insoluble aggregated forms, synaptic proteins and TDP-43 are the markers in the parietal cortex that are most strongly associated with cognitive function. This further substantiates the relevance of investigating these markers to understand the pathogenesis of AD and develop therapeutic tools.

Indexed as

CognitionAgedAged, 80 and overAlzheimer DiseaseAmyloid beta-PeptidesAutopsyBiomarkersCognitive DysfunctionFemaleHumansLongitudinal StudiesMaleNeurofibrillary TanglesNeuropsychological TestsParietal LobePostmortem ChangesAmyloid beta-PeptidesBiomarkerstau ProteinsAlzheimer diseaseAmyloid-βMild cognitive impairmentParietal cortexPostmortemSynaptic proteinsTau.

Identifiers

PMID28158844
PMCPMC7526851
OpenAlexW2585490395

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.