期刊
BIOCHEMICAL SOCIETY TRANSACTIONS
卷 30, 期 -, 页码 552-557出版社
PORTLAND PRESS LTD
DOI: 10.1042/BST0300552
关键词
Alzheimer's disease; amyloid beta-protein; long-term protentiation; neurotoxicity; oligomerization
资金
- NIA NIH HHS [AG05134] Funding Source: Medline
Despite extensive genetic and animal modelling data that support a central role for the amyloid beta-protein (Abeta) in the genesis of Alzheimer's disease, the specific form(s) of Abeta which causes injury to neurons in vivo has not been identified. In the present study, we examine the importance of soluble, pre-fibrillar assemblies of Abeta as mediators of neurotoxicity. Specifically, we review the role of cell-derived SDS-stable oligomers, their blocking of hippocampal long-term potentiation in vivo and the finding that this blocking can be prevented by prior treatment of oligomer-producing cells with gamma-secretase inhibitors.
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