The Apolipoprotein E Antagonistic Pleiotropy Hypothesis: Review and Recommendations

Research on apolipoprotein E (APOE) has consistently revealed a relationship between the gene's ε4 allele and risk for development of Alzheimer's disease (AD). However, research with younger populations of ε4 carriers has suggested that the APOE ε4 allele may in fact be beneficial in earli...

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Main Authors: Tuminello, Elizabeth R., Han, S. Duke
Format: Online
Language:English
Published: SAGE-Hindawi Access to Research 2011
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3056453/
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spelling pubmed-30564532011-03-21 The Apolipoprotein E Antagonistic Pleiotropy Hypothesis: Review and Recommendations Tuminello, Elizabeth R. Han, S. Duke Review Article Research on apolipoprotein E (APOE) has consistently revealed a relationship between the gene's ε4 allele and risk for development of Alzheimer's disease (AD). However, research with younger populations of ε4 carriers has suggested that the APOE ε4 allele may in fact be beneficial in earlier ages and may only confer risk of cognitive decline later in life. Accordingly, we and others have proposed that APOE may represent an example of antagonistic pleiotropy. Antagonistic pleiotropy is an evolutionary biology concept that proposes certain genes or alleles that may differentially impact fitness during different life stages. We critically review this hypothesis in light of new research of the impact of APOE on cognition and neural integrity across the lifespan. We provide recommendations for the revision of the antagonistic pleiotropy hypothesis of APOE and suggest important avenues for future research in this area. SAGE-Hindawi Access to Research 2011-02-24 /pmc/articles/PMC3056453/ /pubmed/21423560 http://dx.doi.org/10.4061/2011/726197 Text en Copyright © 2011 E. R. Tuminello and S. D. Han. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Tuminello, Elizabeth R.
Han, S. Duke
spellingShingle Tuminello, Elizabeth R.
Han, S. Duke
The Apolipoprotein E Antagonistic Pleiotropy Hypothesis: Review and Recommendations
author_facet Tuminello, Elizabeth R.
Han, S. Duke
author_sort Tuminello, Elizabeth R.
title The Apolipoprotein E Antagonistic Pleiotropy Hypothesis: Review and Recommendations
title_short The Apolipoprotein E Antagonistic Pleiotropy Hypothesis: Review and Recommendations
title_full The Apolipoprotein E Antagonistic Pleiotropy Hypothesis: Review and Recommendations
title_fullStr The Apolipoprotein E Antagonistic Pleiotropy Hypothesis: Review and Recommendations
title_full_unstemmed The Apolipoprotein E Antagonistic Pleiotropy Hypothesis: Review and Recommendations
title_sort apolipoprotein e antagonistic pleiotropy hypothesis: review and recommendations
description Research on apolipoprotein E (APOE) has consistently revealed a relationship between the gene's ε4 allele and risk for development of Alzheimer's disease (AD). However, research with younger populations of ε4 carriers has suggested that the APOE ε4 allele may in fact be beneficial in earlier ages and may only confer risk of cognitive decline later in life. Accordingly, we and others have proposed that APOE may represent an example of antagonistic pleiotropy. Antagonistic pleiotropy is an evolutionary biology concept that proposes certain genes or alleles that may differentially impact fitness during different life stages. We critically review this hypothesis in light of new research of the impact of APOE on cognition and neural integrity across the lifespan. We provide recommendations for the revision of the antagonistic pleiotropy hypothesis of APOE and suggest important avenues for future research in this area.
publisher SAGE-Hindawi Access to Research
publishDate 2011
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3056453/
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