Differential effects of ApoE isoforms on dendritic spines in vivo: Linking an Alzheimer’s disease risk factor with synaptic alterations

Basak JM, Kim J (2010). J Neurosci, 30(13):4526-7 Read More

Abstract

The ε4 allele of apolipoprotein E (APOE) is the strongest genetic risk factor for the development of Alzheimer’s disease (AD). Accumulation of amyloid-β (Aβ) is hypothesized to initiate synaptic and neuronal dysfunction that ultimately lead to neuronal cell death in AD, and several lines of evidence strongly suggest that the differential effects of apoE isoforms on Aβ aggregation and/or clearance plays a major role in AD pathogenesis. However, the apoE isoforms could influence the risk for AD via other mechanisms as well. For example, different apoE isoforms might produce differences in synaptic structure and function that make neuronal cells more susceptible to the toxic insults that occur with AD.

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Posted on November 14, 2010
Posted in: HPAN, Neurodegeneration, Publications, Therapeutics & Diagnostics Authors: