作者: Katsuhiko Yanagisawa
DOI: 10.1111/J.1471-4159.2010.07006.X
关键词:
摘要: One of the key questions regarding pathogenesis Alzheimer's disease (AD) is how amyloid β-protein (Aβ), a proteinaceous component senile plaques, starts to assemble into fibrils in brain. A body evidence growing suggest that Aβ binds ganglioside on neuronal membranes, and then, converted an endogenous seed with altered conformation (ganglioside-bound Aβ, GAβ) for fibril formation Notably, risk factors development AD, including aging apolipoprotein E4, likely facilitate clusters lipid raft-like membrane microdomains at pre-synaptic terminals, which provide favorable milieu GAβ generation. Furthermore, it has also been suggested endocytic pathway abnormality neurons involved clusters. In this review, nature gangliosides behave leading generation are discussed.