期刊
NEUROBIOLOGY OF AGING
卷 26, 期 9, 页码 1235-1244出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2005.05.022
关键词
Alzheimer; amyloid; synapse; endosome; multivesicular body; ubiquitin; proteasome
资金
- NINDS NIH HHS [NS045677] Funding Source: Medline
Plaques are a defining neuropathological hallmark of Alzheimer's disease (AD) and the major constituent of plaques, the P-amyloid peptide (A beta), is considered to play an important role in the pathophysiology of AD. But the biological origin of A beta plaques and the mechanism whereby A beta is involved in pathogenesis have been unknown. A beta plaques were thought to form from the gradual accumulation and aggregation of secreted A beta in the extracellular space. More recently, the accumulation of A beta has been demonstrated to occur within neurons with AD pathogenesis. Moreover, intraneuronal A beta accumulation has been reported to be critical in the synaptic dysfunction, cognitive dysfunction and the formation of plaques in AD. Here we provide a historical overview on the origin of plaques and a discussion on potential biological and therapeutic implications of intraneuronal A beta accumulation for AD. (c) 2005 Published by Elsevier Inc.
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