Evidence map›Paper›PMID 30927700›Full record

ArticleNeurobiology of aging2019

Hippocampal gene expression patterns linked to late-life physical activity oppose age and AD-related transcriptional decline.

Nicole C Berchtold, G Aleph Prieto, Michael Phelan, Daniel L Gillen, Pierre Baldi, David A Bennett, Aron S Buchman, Carl W Cotman

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neurobiology of aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 10% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
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  19. Vigorous, regular physical exercise may slow disease progression in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023
    Article
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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

8 authors at 2 institutions in 1 country.

Nicole C BerchtoldInstitute for Memory Impairments and Neurological Disorders, University of California-Irvine, Irvine, CA, USA. Electronic address: nberchto@uci.edu.
G Aleph PrietoInstitute for Memory Impairments and Neurological Disorders, University of California-Irvine, Irvine, CA, USA.
Michael PhelanDepartment of Statistics, University of California, Irvine, CA, USA.
Daniel L GillenStatistics Department, University of California, Irvine, CA, USA.
Pierre BaldiInstitute for Genomics and Bioinformatics, School of Information and Computer Sciences, University of California, Irvine, CA, USA.
David A BennettDepartment of Neurological Sciences, Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL, USA.
Aron S BuchmanDepartment of Neurological Sciences, Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL, USA.
Carl W CotmanInstitute for Memory Impairments and Neurological Disorders, University of California-Irvine, Irvine, CA, USA; Department of Neurology, University of California-Irvine, Irvine, CA, USA.
University of California, Irvine · USRush University Medical Center · US

Funding

Univ.of Calif., Irvine Cancer Center Support GrantP30CA062203 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI Melanie Funes · 1994 to 2026
$57.9M
EPIDEMIOLOGY OF NEURAL RESERVE AND NEUROBIOLOGY IN AGINGR01AG017917 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BENNETT, DAVID ALAN · 2001 to 2023
$43.3M
UC Irvine Alzheimer's Disease Research Center Induced Pluripotent Stem Cell CoreP50AG016573 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI LAFERLA, FRANK M · 2000 to 2019
$37.0M
TISSUE REPOSITORY COREP01AG000538 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI LAFERLA, FRANK M · 1985 to 2018
$24.8M
RISK FACTORS, PATHOLOGY, AND CLINICAL EXPRESSIONS OF ADR01AG015819 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BENNETT, DAVID ALAN · 1998 to 2024
$21.4M
Epigenetic suppression of histone methylation reverses age and AD-related cognitive declineRF1AG057558 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI WOOD, MARCELO ANDRES · 2018 to 2018
$3.8M
Exercise-induced epigenetic mechanisms underlying neuronal plasticity and cognitionR01AG051807 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI COTMAN, CARL WAYNE, WOOD, MARCELO ANDRES · 2016 to 2020
$3.1M
The Clinical Profile of Parkinson's Disease (PD) PathologyR01NS078009 · NINDS · RUSH UNIVERSITY MEDICAL CENTER · PI BUCHMAN, ARON S · 2012 to 2016
$2.4M
Gene Expression, Compensation Mechanisms, and Successful Cognitive AgingR01AG034667 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI COTMAN, CARL WAYNE · 2009 to 2013
$1.7M
NCI NIH HHS P30 CA062203NIA NIH HHS P01 AG000538NIA NIH HHS P50 AG016573NIA NIH HHS R01 AG015819NIA NIH HHS R01 AG017917NIA NIH HHS R01 AG034667NIA NIH HHS R01 AG051807NIA NIH HHS RF1 AG057558NINDS NIH HHS R01 NS078009
6 · The paper itself

Abstract

Exercise has emerged as a powerful variable that can improve cognitive function and delay age-associated cognitive decline and Alzheimer's disease (AD); however, the underlying mechanisms are poorly understood. To determine if protective mechanisms may occur at the transcriptional level, we used microarrays to investigate the relationship between physical activity levels and gene expression patterns in the cognitively intact aged human hippocampus. In parallel, hippocampal gene expression patterns associated with aging and AD were assessed using publicly available microarray data profiling hippocampus from young (20-59 years), cognitively intact aging (73-95 years) and age-matched AD cases. To identify "anti-aging/AD" transcription patterns associated with physical activity, probesets significantly associated with both physical activity and aging/AD were identified and their directions of expression change in each condition were compared. Remarkably, of the 2210 probesets significant in both data sets, nearly 95% showed opposite transcription patterns with physical activity compared with aging/AD. The majority (>70%) of these anti-aging/AD genes showed increased expression with physical activity and decreased expression in aging/AD. Enrichment analysis of the anti-aging/AD genes showing increased expression in association with physical activity revealed strong overrepresentation of mitochondrial energy production and synaptic function, along with axonal function and myelin integrity. Synaptic genes were notably enriched for synaptic vesicle priming, release and recycling, glutamate and GABA signaling, and spine plasticity. Anti-aging/AD genes showing decreased expression in association with physical activity were enriched for transcription-related function (notably negative regulation of transcription). These data reveal that physical activity is associated with a more youthful profile in the hippocampus across multiple biological processes, providing a potential molecular foundation for how physical activity can delay age- and AD-related decline of hippocampal function.

Indexed as

Gene ExpressionAdultAgedAged, 80 and overAgingAlzheimer DiseaseAxonsCognitionEnergy MetabolismExerciseHippocampusHumansMicroarray AnalysisMiddle AgedMitochondriaNeuronal PlasticityAxonExerciseMicroarrayMitochondriaMyelinPlasticitySynaptic vesicle traffickingWhite matter

Identifiers

PMID30927700
PMCPMC6901108
OpenAlexW2916730789

What OpenQuestion 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 OpenQuestion graph.