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Education counteracts the genetic risk of Alzheimer’s disease without an interaction effect

BACKGROUND: Alzheimer’s disease (AD) is a major cause of disability and mortality in older adults. This study aimed to investigate the association of AD with education and genetic factors. METHODS: We conducted a prospective cohort study using data from the UK Biobank. Genetic risk was assessed usin...

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Autores principales: Li, Xuping, Zhang, Yushi, Zhang, Chengcheng, Zheng, Ying, Liu, Ruilin, Xiao, Shuiyuan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10471486/
https://www.ncbi.nlm.nih.gov/pubmed/37663829
http://dx.doi.org/10.3389/fpubh.2023.1178017
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author Li, Xuping
Zhang, Yushi
Zhang, Chengcheng
Zheng, Ying
Liu, Ruilin
Xiao, Shuiyuan
author_facet Li, Xuping
Zhang, Yushi
Zhang, Chengcheng
Zheng, Ying
Liu, Ruilin
Xiao, Shuiyuan
author_sort Li, Xuping
collection PubMed
description BACKGROUND: Alzheimer’s disease (AD) is a major cause of disability and mortality in older adults. This study aimed to investigate the association of AD with education and genetic factors. METHODS: We conducted a prospective cohort study using data from the UK Biobank. Genetic risk was assessed using a polygenic risk score for AD. The educational level was categorized as either low, intermediate, or high. AD was defined using the International Classification of Diseases and Related Health Problems, 10th revision. Logistic regression models were used to investigate the independent and combined effects of genetic factors and educational levels on the risk of AD. RESULTS: We included 318,535 participants in this study (age: 56.53 ± 8.09 years; male: 44.81%). Compared with a low genetic risk, a high genetic risk was associated with a significantly greater risk of AD (OR = 7.09, 95% CI: 6.09–8.26). A high educational level was associated with a 30% lower risk of AD compared with a low educational level (OR = 0.70, 95% CI: 0.60–0.81). Combining genetic risk and education categories, individuals with a low genetic risk and high educational level had a more than 90% (OR = 0.09, 95% CI: 0.05–0.16) lower risk of AD compared to those with a high genetic risk and low educational level. There was no significant interaction between genetic risk and educational level regarding AD risk (p for interaction = 0.359). CONCLUSION: Education counteracts the genetic risk of AD, without an interaction effect. Increasing education to reduce the incidence of AD is of same importance across individuals with different genetic risk.
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spelling pubmed-104714862023-09-02 Education counteracts the genetic risk of Alzheimer’s disease without an interaction effect Li, Xuping Zhang, Yushi Zhang, Chengcheng Zheng, Ying Liu, Ruilin Xiao, Shuiyuan Front Public Health Public Health BACKGROUND: Alzheimer’s disease (AD) is a major cause of disability and mortality in older adults. This study aimed to investigate the association of AD with education and genetic factors. METHODS: We conducted a prospective cohort study using data from the UK Biobank. Genetic risk was assessed using a polygenic risk score for AD. The educational level was categorized as either low, intermediate, or high. AD was defined using the International Classification of Diseases and Related Health Problems, 10th revision. Logistic regression models were used to investigate the independent and combined effects of genetic factors and educational levels on the risk of AD. RESULTS: We included 318,535 participants in this study (age: 56.53 ± 8.09 years; male: 44.81%). Compared with a low genetic risk, a high genetic risk was associated with a significantly greater risk of AD (OR = 7.09, 95% CI: 6.09–8.26). A high educational level was associated with a 30% lower risk of AD compared with a low educational level (OR = 0.70, 95% CI: 0.60–0.81). Combining genetic risk and education categories, individuals with a low genetic risk and high educational level had a more than 90% (OR = 0.09, 95% CI: 0.05–0.16) lower risk of AD compared to those with a high genetic risk and low educational level. There was no significant interaction between genetic risk and educational level regarding AD risk (p for interaction = 0.359). CONCLUSION: Education counteracts the genetic risk of AD, without an interaction effect. Increasing education to reduce the incidence of AD is of same importance across individuals with different genetic risk. Frontiers Media S.A. 2023-08-17 /pmc/articles/PMC10471486/ /pubmed/37663829 http://dx.doi.org/10.3389/fpubh.2023.1178017 Text en Copyright © 2023 Li, Zhang, Zhang, Zheng, Liu and Xiao. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Public Health
Li, Xuping
Zhang, Yushi
Zhang, Chengcheng
Zheng, Ying
Liu, Ruilin
Xiao, Shuiyuan
Education counteracts the genetic risk of Alzheimer’s disease without an interaction effect
title Education counteracts the genetic risk of Alzheimer’s disease without an interaction effect
title_full Education counteracts the genetic risk of Alzheimer’s disease without an interaction effect
title_fullStr Education counteracts the genetic risk of Alzheimer’s disease without an interaction effect
title_full_unstemmed Education counteracts the genetic risk of Alzheimer’s disease without an interaction effect
title_short Education counteracts the genetic risk of Alzheimer’s disease without an interaction effect
title_sort education counteracts the genetic risk of alzheimer’s disease without an interaction effect
topic Public Health
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10471486/
https://www.ncbi.nlm.nih.gov/pubmed/37663829
http://dx.doi.org/10.3389/fpubh.2023.1178017
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