The overall contribution of modifiable lifestyle, adiposity, socioeconomic status, and health conditions occurring before dementia, to the association between ε4 genotype and the development of all-cause dementia was quantified.
Abstract
Dementia is a major public health challenge, and Apolipoprotein E (APOE) ε4 is strongly associated with all-cause dementia, particularly Alzheimer's disease (AD). We aim to quantify the overall contribution of modifiable lifestyle, adiposity, socioeconomic status (SES), and health conditions occurring before dementia, to the association between ε4 genotype and the development of all-cause dementia, with AD examined as a major subtype. A population cohort study of 181,006 white UK Biobank participants aged ≥ 55 years at baseline was conducted, to examine the associations between APOE ε4 and all-cause dementia, and specifically AD, including modification and mediation role of lifestyle factors, adiposity, SES, and health conditions occurring before dementia. All risk factors, except for high alcohol intake, low diet quality, and phenotypic obesity, were associated with higher risk of all-cause dementia. The interaction contributions of lifestyle, adiposity, SES, and health conditions occurring before dementia varied by sex and dementia type. Low educational attainment had the strongest interaction effects with the association of APOE ε4 carriers and AD/all-cause dementia (up to 32.1%). In women, high deprivation level, abnormal sleep duration, anxiety, and depression showed interaction effects with APOE genotype (5-11.6%) as well. Phenotypic adiposity was associated with an increased risk of dementia among APOE ε4 non-carriers, but with a reduced risk among APOE ε4 carriers. Educational attainment explained a meaningful proportion of the APOE ε4 association with dementia. The strength of the association between APOE ε4 and dementia differed by risk factors and sex.
In this Indian cohort, APOE ε4 homozygosity reflects increased susceptibility and familial aggregation of AD but does not confer a more severe or distinct phenotype, suggesting ancestry- specific expression of APOE ε4 gene-dose effects.
Pratibha Vinod, C. Arampady, Somdatta Sen et al.· Neurodegenerative Disease Ma...· 0 citations
BackgroundThe strongest genetic risk factor for development of Alzheimer's disease (AD) and/or AD-related dementias is the ε4 allele in the apolipoprotein E (APOE) gene, though the frequency and impact of this variant on cognitive decline can vary across populations. Vascular and metabolic disorders (e.g., hypertension...
Amanda E. Tucker, Robert C. Barber, Zheng-Yang Zhou et al.· Journal of Alzheimer's Disea...· 0 citations
OBJECTIVE
We examined how cardiovascular health (CVH), measured by Life's Essential 8 (LE8), and genetic risk are jointly associated with risks of mild cognitive impairment (MCI), dementia, and related cognitive outcomes in people with diabetes.
RESEARCH DESIGN AND METHODS
We analyzed 41,374 participants without deme...
Xiu Wu, Y. Zu, You Lu et al.· Diabetes Care· 0 citations
Attenuated associations in older-old adults may reflect survivor bias, while stronger associations in APOE ε4 carriers are consistent with gene-environment interactions, which are consistent with gene-environment interactions.
Yang Kong, Xian Li, Rui-Qian Guan et al.· Alzheimer Disease and Associ...· 0 citations
Background Whether plasma protein associations with Alzheimer’s disease (AD) differ by genetic risk remains unclear. Methods We studied 18,212 UK Biobank participants aged ≥ 60 years with Olink Explore 3072 proteomic data, APOE genotypes, and AD polygenic risk scores. Protein-by-genetic risk interactions were screened,...
Yuan-Ming Leng, Hui-Tong Ding, Jian Yang et al.· Research Square· 0 citations
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