Evidence map›Paper›PMID 39350213›Full record

ArticleBMC medicine2024

Associations of combined accelerated biological aging and genetic susceptibility with incident dementia: a prospective study in the UK Biobank.

Zirong Ye, Haoxiang Lang, Zishan Xie, Siyu Duan, Bihao Peng, Xiaochun Chen, Ya Fang, Jiawei Xin

Abstract read
In one paragraph

Article in BMC medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Article
  2. Multivariate Random Forests for Cross-Modal Multi-Omics Integration.bioRxiv : the preprint server for biology · 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

8 authors.

Zirong YeKey Laboratory of Health Technology Assessment of Fujian Province, School of Public Health, Xiamen University, Xiang'an Nan Road, Xiang'an District, Xiamen, Fujian, 361102, China.
Haoxiang LangKey Laboratory of Health Technology Assessment of Fujian Province, School of Public Health, Xiamen University, Xiang'an Nan Road, Xiang'an District, Xiamen, Fujian, 361102, China.
Zishan XieCollege of Mechanical and Electrical Engineering, Fujian Agriculture and Forestry University, No. 63, Xiyuan Gong Road, Minhou County, Fuzhou, Fujian, 350000, China.
Siyu DuanKey Laboratory of Health Technology Assessment of Fujian Province, School of Public Health, Xiamen University, Xiang'an Nan Road, Xiang'an District, Xiamen, Fujian, 361102, China.
Bihao PengDepartment of Neurology, Fujian Medical University Union Hospital, Fujian Key Laboratory of Molecular Neurology and Institute of Neuroscience, Fujian Medical University, No.29, Xinquan Road, Gulou District, Fuzhou, Fujian Province, 350000, China.
Xiaochun ChenDepartment of Neurology, Fujian Medical University Union Hospital, Fujian Key Laboratory of Molecular Neurology and Institute of Neuroscience, Fujian Medical University, No.29, Xinquan Road, Gulou District, Fuzhou, Fujian Province, 350000, China.
Ya FangKey Laboratory of Health Technology Assessment of Fujian Province, School of Public Health, Xiamen University, Xiang'an Nan Road, Xiang'an District, Xiamen, Fujian, 361102, China. fangya@xmu.edu.cn.
Jiawei XinDepartment of Neurology, Fujian Medical University Union Hospital, Fujian Key Laboratory of Molecular Neurology and Institute of Neuroscience, Fujian Medical University, No.29, Xinquan Road, Gulou District, Fuzhou, Fujian Province, 350000, China. xinjw@fjmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAccelerated biological aging has been verified to be a critical risk factor for a number of age-related diseases, but its role in dementia remained unclear. Whether it modified the effects of genetic factors was also unknown. This study evaluated the associations between accelerated biological aging and dementia and the moderating role of accelerated biological aging in the genetic susceptibility to the disease.

methodsWe included 200,731 participants in the UK biobank. Nine clinical blood biomarkers and chronological age were used to calculate Phenotypic age acceleration (PhenoAgeAccel), which is a novel indicator for accelerated biological aging. The associations of PhenoAgeAccel with dementia, both young-onset and late-onset dementia, were assessed by Cox proportional hazard models. Apolipoprotein E (APOE) alleles and polygenic risk scores (PRS) were used to evaluate the genetic risk of dementia. The interactions between genetic susceptibility and biological aging were tested on both multiplicative and additive scales.

resultsThese findings showed individuals who were in the highest quartile of PhenoAgeAccel had a higher risk with incidence of dementia compared to individuals in the lowest quartile of PhenoAgeAccel (HR: 1.145 (95% CI: 1.050, 1.249)). Individuals with biologically older had a higher risk of dementia than individuals with biologically younger (HR: 1.069 (95% CI: 1.004, 1.138)). Furthermore, compared to individuals with biologically younger and low APOE ε4-related genetic risk, individuals with biologically younger and high APOE ε4-related genetic risk (HR:3.048 (95% CI: 2.811, 3.305)) had a higher risk of dementia than individuals with biologically older and high APOE ε4-related genetic risk (HR: 2.765 (95% CI: 2.523, 3.029)). Meanwhile, referring to low dementia PRS and biologically younger, the risk of dementia increased by 72.7% (HR: 1.727 (95% CI: 1.538, 1.939) in the biologically younger and high PRS group and 58.7% (HR: 1.587 (95% CI: 1.404, 1.793) in the biologically older and high PRS group, respectively. The negative interactions between PhenoAgeAccel with APOE ε4 and PRS were also tested on the additive scale.

conclusionsAccelerated biological aging could bring the extra risk of dementia but attenuate the effects of genetic risk on dementia. These findings provide insights for precise prevention and intervention of dementia.

Indexed as

AgingBiological Specimen BanksDementiaGenetic Predisposition to DiseaseAdultAgedAged, 80 and overApolipoproteins EFemaleHumansIncidenceMaleMiddle AgedProspective StudiesRisk FactorsUK BiobankApolipoproteins EAccelerated biological agingApolipoprotein EAttributable proportionDementiaPolygenetic risk scoreRelative excess riskUK Biobank

Identifiers

PMID39350213
PMCPMC11443929

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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.