Evidence map›Paper›PMID 40181791›Full record

ArticleCirculation2025

Genetic and Lifestyle Risks for Coronary Artery Disease and Long-Term Risk of Incident Dementia Subtypes.

Arisa Sittichokkananon, Victoria Garfield, Scott T Chiesa

Abstract read
In one paragraph

Article in Circulation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

  1. Associations of long-term exposure to source-specific PMEuropean archives of psychiatry and clinical neuroscience · 2026
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  2. Article
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  6. The enigma of vascular dementia: current state and emerging perspectives.Journal of neural transmission (Vienna, Austria : 1996) · 2026
    Review
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  12. MEDICATION EXPOSURE AND NEURODEGENERATIVE DISEASE RISK ACROSS NATIONAL BIOBANKS.medRxiv : the preprint server for health sciences · 2025
    Article
  13. Review
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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

3 authors.

Arisa SittichokkananonPrincess Srisavangavadhana College of Medicine, Chulabhorn Royal Academy, Bangkok, Thailand (A.S.).
Victoria GarfieldDepartment of Pharmacology & Therapeutics, Institute of Systems, Molecular, & Integrative Biology, University of Liverpool, UK (V.G.).ORCID 0000-0002-5127-0890
Scott T ChiesaDepartment of Population Science and Experimental Medicine, Institute of Cardiovascular Science, UCL, London, UK (A.S., S.T.C.).ORCID 0000-0003-4323-2189

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundShared genetic and lifestyle risk factors may underlie the development of both coronary artery disease (CAD) and dementia. We examined whether an increased genetic risk for CAD is associated with long-term risk of developing all-cause, Alzheimer's, or vascular dementia, and investigated whether differences in potentially modifiable lifestyle factors in the mid- to late-life period may attenuate this risk.

methodsA prospective cohort study of 365 782 participants free from dementia for at least 5 years after baseline assessment was conducted within the UK Biobank cohort. Genetic risk was assessed using a genomewide polygenic risk score (PRS) for CAD and lifestyle risk using a modified version of the American Heart Association's Life's Essential 8 Lifestyle Risk Score (LRS). Higher values for both scores were deemed to represent increased risk. Primary outcomes were incident all-cause, Alzheimer's, and vascular dementia diagnoses obtained from self-report and electronic health records. Secondary outcomes were neuroimaging phenotypes measured in 32 028 participants recalled for magnetic resonance imaging. Sensitivity analyses were conducted to test the extent by which biological and behavioral risk factors contributed to observed associations.

resultsA total of 8870 cases of all-cause dementia were observed over a median 13.9-year follow-up. Both genetic (PRS) and lifestyle (LRS) risk scores for CAD were associated with a modestly elevated risk of all-cause dementia (subhazard ratio per SD increase, 1.10 [1.08, 1.12],

conclusionsIndividuals who are genetically predisposed to developing CAD also face an increased risk of developing dementia in old age. This risk is reduced in those demonstrating healthy lifestyle profiles earlier in the lifespan, particularly in those who may be at an increased risk of developing dementia caused by an underlying vascular pathology.

Indexed as

Coronary Artery DiseaseDementiaLife StyleAgedDementia, VascularFemaleGenetic Predisposition to DiseaseHumansIncidenceMaleMiddle AgedProspective StudiesRisk FactorsAlzheimer’s diseasedementiadementia, vascularheart disease risk factors

Identifiers

PMID40181791
PMCPMC12036788

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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.