期刊
JOURNAL OF ALZHEIMERS DISEASE
卷 16, 期 2, 页码 225-233出版社
IOS PRESS
DOI: 10.3233/JAD-2009-0951
关键词
Alzheimer's disease; amyloid; calcium; neurotoxicity; synaptic plasticity
Although many of the biochemical mechanisms which regulate production or clearance of the amyloid-beta protein (A beta) of Alzheimer's disease (AD) are now well understood, the mechanism of A beta neurotoxicity remains unclear. A number of studies have shown that A beta can disrupt neuronal Ca2+ homeostasis by inducing influx of extracellular Ca2+ into the neuronal cytoplasm. Ca2+ is known to play an important role in neuronal excitability, synaptic plasticity and neurotoxicity. Therefore, A beta-induced Ca2+ dysregulation may contribute to many of the cognitive and neuropathologic features of AD. In vitro studies show that A beta can increase ion permeability in lipid membranes. This increased permeability is reportedly associated with the formation of artificial ion pores formed from A beta oligomers. However, a number of other studies show that A beta can activate endogenous ion channels on the cell surface. There is also increasing evidence that presenilin mutations alter intracellular Ca2+ stores. It is likely that elucidation of the mechanism by which A beta and presenilin cause Ca2+ dysregulation in neurons will help to identify new drug targets for the treatment of AD.
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