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Apolipoprotein E influences neuronal death and repair

Research output: Contribution to journalArticle

Original languageUndefined/Unknown
Pages (from-to)171-178
Number of pages8
JournalInternational Congress Series
Volume1252
DOIs
Publication statusPublished - 2003
EventInternational Symposium: Molecular Mechanism and Epochal Therapeutics of ischemic Stroke and Dementia. - Okayama, Japan
Duration: 18 Oct 200220 Oct 2002

Abstract

The ε4 allele of apolipoprotein E is a major risk factor for Alzheimer's disease (AD) and is associated with a poor outcome after acute brain injury by what appears to be common mechanisms. The multiplicity of the roles of apoE within the central nervous system is currently being elucidated using transgenic mice (APOE knockout with or without human APOE ε3 and ε4 alleles). ApoE mediates neuronal protection, repair and remodelling via a number of mechanisms including antioxidant effects, interactions with oestrogen and modulation of synaptodendritic proteins. In all of the different roles proposed, there are marked apoE-isoform specific differences although the most important mechanism(s) remains to be clarified. ApoE-isoform specific differences underlie a genetically determined susceptibility to outcome from acute brain injury and to AD with APOE ε4 conferring relative vulnerability. This review focuses on the utility of animal models and transgenic mice to understand the mechanisms underlying the genetic susceptibility conferred by the APOE ε4 allele.

ID: 4115807