Interaction between genetic predisposition, smoking, and dementia risk: a population-based cohort study

Abstract We evaluated whether the association between cigarette smoking and dementia risk is modified by genetic predisposition including apolipoprotein E (APOE) genotype and polygenic risk (excluding the APOE region). We included 193,198 UK Biobank participants aged 60–73 years without dementia at...

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Autores principales:	Na Zhang, Janice M. Ranson, Zhi-Jie Zheng, Eilis Hannon, Zhenwei Zhou, Xuejun Kong, David J. Llewellyn, Daniel A. King, Jie Huang
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/b6daf5cefaee4cfdb8f7143e65149d47
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spelling	oai:doaj.org-article:b6daf5cefaee4cfdb8f7143e65149d472021-12-02T17:12:17ZInteraction between genetic predisposition, smoking, and dementia risk: a population-based cohort study10.1038/s41598-021-92304-x2045-2322https://doaj.org/article/b6daf5cefaee4cfdb8f7143e65149d472021-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-92304-xhttps://doaj.org/toc/2045-2322Abstract We evaluated whether the association between cigarette smoking and dementia risk is modified by genetic predisposition including apolipoprotein E (APOE) genotype and polygenic risk (excluding the APOE region). We included 193,198 UK Biobank participants aged 60–73 years without dementia at baseline. Of non-APOE-ε4 carriers, 0.89% (95% CI 0.73–1.08%) current smokers developed dementia compared with 0.49% (95% CI 0.44–0.55%) of never smokers (adjusted HR 1.78; 95% CI 1.39–2.29). In contrast, of one APOE-ε4 allele carriers, 1.69% (95% CI 1.31–2.12%) current smokers developed dementia compared with 1.40% (95% CI 1.25–1.55%) of never smokers (adjusted HR 1.06; 95% CI 0.77–1.45); of two APOE-ε4 alleles carriers, 4.90% (95% CI 2.92–7.61%) current smokers developed dementia compared with 3.87% (95% CI 3.11–4.74%) of never smokers (adjusted HR 0.94; 95% CI 0.49–1.79). Of participants with high polygenic risk, 1.77% (95% CI 1.35–2.27%) current smokers developed dementia compared with 1.05% (95% CI 0.91–1.21%) of never smokers (adjusted HR 1.63; 95% CI 1.16–2.28). A significant interaction was found between APOE genotype and smoking status (P = 0.002) while no significant interaction was identified between polygenic risk and smoking status (P = 0.25). APOE genotype but not polygenic risk modified the effect of smoking on dementia risk.Na ZhangJanice M. RansonZhi-Jie ZhengEilis HannonZhenwei ZhouXuejun KongDavid J. LlewellynDaniel A. KingJie HuangNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-10 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Na Zhang Janice M. Ranson Zhi-Jie Zheng Eilis Hannon Zhenwei Zhou Xuejun Kong David J. Llewellyn Daniel A. King Jie Huang Interaction between genetic predisposition, smoking, and dementia risk: a population-based cohort study
description	Abstract We evaluated whether the association between cigarette smoking and dementia risk is modified by genetic predisposition including apolipoprotein E (APOE) genotype and polygenic risk (excluding the APOE region). We included 193,198 UK Biobank participants aged 60–73 years without dementia at baseline. Of non-APOE-ε4 carriers, 0.89% (95% CI 0.73–1.08%) current smokers developed dementia compared with 0.49% (95% CI 0.44–0.55%) of never smokers (adjusted HR 1.78; 95% CI 1.39–2.29). In contrast, of one APOE-ε4 allele carriers, 1.69% (95% CI 1.31–2.12%) current smokers developed dementia compared with 1.40% (95% CI 1.25–1.55%) of never smokers (adjusted HR 1.06; 95% CI 0.77–1.45); of two APOE-ε4 alleles carriers, 4.90% (95% CI 2.92–7.61%) current smokers developed dementia compared with 3.87% (95% CI 3.11–4.74%) of never smokers (adjusted HR 0.94; 95% CI 0.49–1.79). Of participants with high polygenic risk, 1.77% (95% CI 1.35–2.27%) current smokers developed dementia compared with 1.05% (95% CI 0.91–1.21%) of never smokers (adjusted HR 1.63; 95% CI 1.16–2.28). A significant interaction was found between APOE genotype and smoking status (P = 0.002) while no significant interaction was identified between polygenic risk and smoking status (P = 0.25). APOE genotype but not polygenic risk modified the effect of smoking on dementia risk.
format	article
author	Na Zhang Janice M. Ranson Zhi-Jie Zheng Eilis Hannon Zhenwei Zhou Xuejun Kong David J. Llewellyn Daniel A. King Jie Huang
author_facet	Na Zhang Janice M. Ranson Zhi-Jie Zheng Eilis Hannon Zhenwei Zhou Xuejun Kong David J. Llewellyn Daniel A. King Jie Huang
author_sort	Na Zhang
title	Interaction between genetic predisposition, smoking, and dementia risk: a population-based cohort study
title_short	Interaction between genetic predisposition, smoking, and dementia risk: a population-based cohort study
title_full	Interaction between genetic predisposition, smoking, and dementia risk: a population-based cohort study
title_fullStr	Interaction between genetic predisposition, smoking, and dementia risk: a population-based cohort study
title_full_unstemmed	Interaction between genetic predisposition, smoking, and dementia risk: a population-based cohort study
title_sort	interaction between genetic predisposition, smoking, and dementia risk: a population-based cohort study
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/b6daf5cefaee4cfdb8f7143e65149d47
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_version_	1718381457890607104

Interaction between genetic predisposition, smoking, and dementia risk: a population-based cohort study

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