Evidence map›Paper›PMID 41329349›Full record

ArticleJournal of neurology2025

Physical activity and Alzheimer's disease risk across genetic susceptibility: a prospective UK Biobank study using accelerometer data.

Seunghee Na, Kenneth Muir, Artitaya Lophatananon, Yicong Huang, Jongin Lee

Abstract read
In one paragraph

Article in Journal of neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

5 authors.

Seunghee NaDepartment of Neurology, Incheon St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
Kenneth MuirDivision of Population Health, Health Services Research and Primary Care, Faculty of Biology, Medicine and Health, School of Health Sciences, The University of Manchester, Manchester, UK.
Artitaya LophatananonDivision of Population Health, Health Services Research and Primary Care, Faculty of Biology, Medicine and Health, School of Health Sciences, The University of Manchester, Manchester, UK.
Yicong HuangDivision of Population Health, Health Services Research and Primary Care, Faculty of Biology, Medicine and Health, School of Health Sciences, The University of Manchester, Manchester, UK.
Jongin LeeDivision of Population Health, Health Services Research and Primary Care, Faculty of Biology, Medicine and Health, School of Health Sciences, The University of Manchester, Manchester, UK. leejongin@catholic.ac.kr.ORCID http://orcid.org/0000-0003-4337-8444

Funding

HORIZON EUROPE Health 101137301UK Research and Innovation 10103541
6 · The paper itself

Abstract

objectivePhysical activity (PA) has been associated with reduced Alzheimer's disease (AD) risk, but whether protective effects vary across genetic risk levels remains unclear. Previous studies were limited by self-reported PA measures and simplified genetic models. In this study, we aimed to examine the association between accelerometer-measured physical activity and the risk of incident AD in a large population-based cohort, and to explore potential interactions between PA and polygenic risk scores for AD.

methodsWe analyzed 93,578 UK Biobank participants aged 40-70 years with accelerometer data and genome-wide genotyping. PA was measured continuously (milligravity, mg) and dichotomized at the optimal point from maximally selected rank statistics. Genetic risk was assessed using polygenic risk scores (PRS) and APOE ε4 status. Cox models estimated hazard ratios for incident AD across genetic risk strata during median 15.5-year follow-up.

resultsAmong 401 AD cases, high PA reduced risk by 48% (HR 0.517; 95% CI 0300-0.891), while high PRS increased risk nearly twofold (HR 2.423; 95% CI 1.757-3.343). PA's protective association remained consistent across all PRS and APOE ε4 strata. No significant multiplicative or additive interaction was found between PA and genetic risk (RERI = - 0.566, 95% CI - 4.574-3.441). Dose-response analysis revealed maximum benefit with optimal threshold at 21.7 mg corresponding to light-intensity activity.

conclusionObjectively measured PA substantially reduces AD risk regardless of genetic predisposition. Even light-intensity activity provides meaningful protection, supporting PA as a broadly applicable preventive strategy across all genetic risk levels.

Indexed as

Alzheimer DiseaseExerciseGenetic Predisposition to DiseaseAccelerometryAdultAgedApolipoprotein E4Biological Specimen BanksFemaleGenome-Wide Association StudyHumansMaleMiddle AgedMultifactorial InheritanceProspective StudiesRisk FactorsApolipoprotein E4Alzheimer's diseaseAPOE genePhysical activityUK Biobank

Identifiers

PMID41329349
PMCPMC12672744

What Socratic holds

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LicenceCC BY
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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 Socratic graph.