Evidence map›Paper›PMID 40441049›Full record

ArticleNeurobiology of aging2025

Modifiable risk factor profiles moderate the effect of β-amyloid pathology on cognition in aging.

Mohini Bhade, Stefania Pezzoli, Joseph Giorgio, Tyler J Ward, Joseph R Winer, Theresa M Harrison, Susan M Landau, William J Jagust

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neurobiology of aging, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Mohini BhadeDepartment of Neuroscience, University of California, Berkeley, Berkeley, California, USA. Electronic address: mohini_bhade@berkeley.edu.
Stefania PezzoliDepartment of Neuroscience, University of California, Berkeley, Berkeley, California, USA; Molecular Biophysics and Integrated Bioimaging, Lawrence Berkeley National Laboratory, Berkeley, California, USA.
Joseph GiorgioDepartment of Neuroscience, University of California, Berkeley, Berkeley, California, USA; School of Psychological Sciences, College of Engineering, Science and the Environment, University of Newcastle, Newcastle, New South Wales, Australia.
Tyler J WardDepartment of Neuroscience, University of California, Berkeley, Berkeley, California, USA.
Joseph R WinerStanford University School of Medicine, Stanford, California, USA.
Theresa M HarrisonDepartment of Neuroscience, University of California, Berkeley, Berkeley, California, USA.
Susan M LandauDepartment of Neuroscience, University of California, Berkeley, Berkeley, California, USA.
William J JagustDepartment of Neuroscience, University of California, Berkeley, Berkeley, California, USA; Molecular Biophysics and Integrated Bioimaging, Lawrence Berkeley National Laboratory, Berkeley, California, USA.

Funding

Neural and Biochemical Mechanisms of Cognitive AgingR01AG034570 · NIA · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI William J. Jagust · 2009 to 2026
$12.0M
Mechanisms of Alzheimer's Disease Progression in the Aging BrainR01AG062542 · NIA · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI JAGUST, WILLIAM J. · 2019 to 2023
$4.2M
Linking basal forebrain and entorhinal cortex vulnerability to preclinical Alzheimer's diseaseK01AG078443 · NIA · UNIVERSITY OF CALIFORNIA BERKELEY · PI Theresa M. Harrison · 2022 to 2026
$656k
NIA NIH HHS K01 AG078443NIA NIH HHS R01 AG034570NIA NIH HHS R01 AG062542
6 · The paper itself

Abstract

Although modifiable risk factors may account for around 40 % of population variability in dementia risk, the effect of risk factor interrelationships on pathology-cognition relationships is poorly understood. Using risk factor data from a cohort of 203 cognitively normal older adults (73 ± 6.4 years, 56 % female), we used k-means clustering to assign participants to one of three risk-related profiles; namely, positive-active (physical/cognitive activity, education), positive-affective (sleep, depression, personality), and negative multi-domain clusters. Linear mixed-effects models showed an attenuated effect of β-amyloid on non-memory cognition decline in positive profiles (positive-active: β=3.7, p = 0.008, positive-affective: β=3.7, p = 0.007) compared to the negative profile. While a significant entorhinal tau x time effect (p < 0.001) was observed in a model predicting episodic memory decline, cluster membership did not modify this relationship. These findings suggest that different risk profiles moderate pathology-cognition relationships, and highlight the role of groups of modifiable resilience factors in mitigating the effects of β-amyloid deposition.

Indexed as

AgingAmyloid beta-PeptidesCognitionAgedAged, 80 and overCohort StudiesDementiaDepressionEducational StatusFemaleHumansMalePersonalityRisk FactorsSleepAmyloid beta-PeptidesB-amyloidCognitionLifestyleNormal agingResilienceRisk factorTau

Identifiers

PMID40441049
PMCPMC13257327

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Registered trials

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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.