Apolipoprotein E isoform-specific reduction of extracellular amyloid in neuronal cultures

Abstract Both apolipoprotein E (apoE) and amyloid peptides are associated with Alzheimer's disease (AD). Using primary hippocampal neurons, we demonstrate that apoE is capable of reducing potentially toxic extracellular amyloid peptides, likely through a receptor mediated mechanism. We hypothesize that isoform-specific differences in apoE-mediated amyloid clearance and intracellular accumulation may be responsible, at least in part, for the increased number of amyloid plaques observed in apoE ϵ4 allele AD individuals.