title: Apolipoprotein E isoforms and regulation of the innate immune response in brain of patients with Alzheimer's disease.
abstract: The largest genetic risk for late-onset Alzheimer's disease (AD) resides at the apolipoprotein E gene (APOE) locus, which has three common alleles (ɛ2, ɛ3, ɛ4) that encode three isoforms (apoE2, apoE3, apoE4). The very strong association of the APOE ɛ4 allele with AD risk and its role in the accumulation of amyloid β in brains of people and animal models solidify the biological relevance of apoE isoforms but do not provide mechanistic insight. The innate immune response is consistently observed in AD and is a likely contributor to neuronal injury and response to injury. Here we review emerging data showing that apoE isoform regulation of multiple facets of the innate immune response in the brain may alter AD not only through amyloid β-dependent mechanisms, but also through other, amyloid β-independent mechanisms.
authors: Department of Pathology, University of Washington, Seattle, WA, United States.
authors: C Dirk
authors: CD
authors: Keene
authors: Eiron
authors: E
authors: Cudaback
authors: Xianwu
authors: X
authors: Li
authors: Kathleen S
authors: KS
authors: Montine
authors: Thomas J
authors: TJ
authors: Montine
mesh_terms: D000544:Alzheimer Disease / Q000235:genetics* / Q000276:immunology* / Q000378:metabolism; D000818:Animals; D001057:Apolipoproteins E / Q000235:genetics* / Q000276:immunology*; D020022:Genetic Predisposition to Disease; D006801:Humans; D007113:Immunity, Innate / Q000235:genetics* / Q000276:immunology*; D020033:Protein Isoforms / Q000235:genetics / Q000276:immunology
chemical_list: D001057:Apolipoproteins E; D020033:Protein Isoforms