Evidence map›Paper›PMID 28624335›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2017

Neuropathologic features of TOMM40 '523 variant on late-life cognitive decline.

Lei Yu, Michael W Lutz, Jose M Farfel, Robert S Wilson, Daniel K Burns, Ann M Saunders, Philip L De Jager, Lisa L Barnes, Julie A Schneider, David A Bennett

Open access · greenAbstract read
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

25 citing papers in PubMed, 28 citations in OpenAlex.

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  5. Evaluating the association of apolipoprotein E genotype and cognitive resilience in SuperAgers.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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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

10 authors at 4 institutions in 2 countries.

Lei YuRush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL, USA; Department of Neurological Sciences, Rush University Medical Center, Chicago, IL, USA. Electronic address: lei_yu@rush.edu.
Michael W LutzDepartment of Neurology, Duke University School of Medicine, Durham, NC, USA.
Jose M FarfelRush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL, USA; Discipline of Geriatrics, Faculty of Medicine of the University of Sao Paulo, Brazil.
Robert S WilsonRush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL, USA; Department of Neurological Sciences, Rush University Medical Center, Chicago, IL, USA; Department of Behavioral Sciences, Rush University Medical Center, Chicago, IL, USA.
Daniel K BurnsZinfandel Pharmaceuticals, Inc., Research Triangle Park, NC, USA.
Ann M SaundersZinfandel Pharmaceuticals, Inc., Research Triangle Park, NC, USA.
Philip L De JagerCenter for Translational and Computational Neuroimmunology, Department of Neurology, Columbia University Medical Center, New York, NY, USA; Program in Medical and Population Genetics, Broad Institute, Cambridge, MA, USA.
Lisa L BarnesRush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL, USA; Department of Neurological Sciences, Rush University Medical Center, Chicago, IL, USA; Department of Behavioral Sciences, Rush University Medical Center, Chicago, IL, USA.
Julie A SchneiderRush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL, USA; Department of Neurological Sciences, Rush University Medical Center, Chicago, IL, USA.
David A BennettRush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL, USA; Department of Neurological Sciences, Rush University Medical Center, Chicago, IL, USA.
Rush University Medical Center · USResearch Triangle Park Foundation · USBroad Institute · USDuke University · US

Funding

SUPPLEMENT TO RUSH ALZHEIMERS DISEASE CENTER COREP30AG010161 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BENNETT, DAVID ALAN · 1991 to 2020
$49.1M
EPIDEMIOLOGY OF NEURAL RESERVE AND NEUROBIOLOGY IN AGINGR01AG017917 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BENNETT, DAVID ALAN · 2001 to 2023
$43.3M
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
Epidemiologic Study of TDP-43 Pathology in Aging and DementiaR01AG042210 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI SCHNEIDER, JULIE A. · 2012 to 2018
$2.4M
Role of the TOMM40 poly-T variant in the pathogenesis of Alzheimer's diseaseR01AG040370 · NIA · DUKE UNIVERSITY · PI CHIBA-FALEK, ORNIT · 2013 to 2017
$2.2M
NIA NIH HHS P30 AG010161NIA NIH HHS R01 AG015819NIA NIH HHS R01 AG017917NIA NIH HHS R01 AG040370NIA NIH HHS R01 AG042210NIA NIH HHS RF1 AG015819
6 · The paper itself

Abstract

introductionThe study investigated the role of neuropathologies in the relationship between TOMM40 '523 genotype and late-life cognitive decline.

methodsParticipants were community-dwelling older persons who had annual cognitive assessments and brain autopsies after death. Genotyping used DNA from peripheral blood or postmortem brain tissue. Linear mixed models assessed the extent to which the association of '523 genotype with cognitive decline is attributable to neuropathologies.

resultsRelative to ε3/ε3 homozygotes with '523-S/VL or '523-VL/VL genotype, both '523-L carriers and ε3/ε3 homozygotes with '523-S/S genotype had faster cognitive decline. The association of '523-L with cognitive decline was attenuated and no longer significant after controlling for Alzheimer's and other neuropathologies. By contrast, the association of '523-S/S was unchanged. DISCUSSION: There are two distinct TOMM40 '523 signals in relation to late-life cognitive decline. One signal primarily acts through AD and other common neuropathologies, whereas the other operates through a different mechanism.

Indexed as

AgedAged, 80 and overApolipoproteins EBrainCognition DisordersCohort StudiesDiagnosisFemaleGenetic Predisposition to DiseaseGenotypeHumansMaleMembrane Transport ProteinsMitochondrial Precursor Protein Import Complex ProteinsNeuropsychological TestsPolymorphism, GeneticApolipoproteins EMembrane Transport ProteinsMitochondrial Precursor Protein Import Complex ProteinsTOMM40 protein, humanAlzheimer's diseaseAPOELate-life cognitive declineNeuropathologiesTOMM40 '523

Identifiers

PMID28624335
PMCPMC5723540
OpenAlexW2625905165

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.