Human and murine ApoE markedly alters A beta metabolism before and after plaque formation in a mouse model of Alzheimer's disease.
作者： Anne M. Fagan , Melanie Watson , Maia Parsadanian , Kelly R. Bales , Steven M. Paul
关键词:
摘要: The epsilon4 allele of apolipoprotein E (apoE) is a risk factor for Alzheimer's disease (AD), perhaps through effects on amyloid-beta (Abeta) metabolism. Detailed analyses various Abeta parameters in aging APP(V717F+/-) transgenic mice expressing mouse apoE, no or human apoE2, apoE3, apoE4 demonstrate that apoE facilitates, but not required for, fibril formation vivo. Human isoforms markedly delayed deposition relative to with apoE2 (and apoE3 lesser extent) having prolonged ability prevent from converting into fibrillar forms. Isoform-specific levels and neuritic plaque mimicked observed AD (E4 > E3 E2). Importantly, observation an apoE-dependent decrease percent soluble enrichment membrane microdomains prior indicates influences metabolism early the amyloidogenic process provides possible novel mechanism by which affects pathogenesis.
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