期刊
MOLECULAR NEUROBIOLOGY
卷 38, 期 1, 页码 78-100出版社
SPRINGER
DOI: 10.1007/s12035-008-8036-x
关键词
neurodegenerative disease; calpain; cerebral ischemia; Alzheimer's; Parkinson's; Huntington's; amylotrophic lateral sclerosis; multiple sclerosis; prion-related encephalopathy; excitotoxicity; calcium
资金
- NINDS NIH HHS [R01 NS044178, R01 NS036736-11, R01 NS056118-03, R01 NS045048, R01 NS056118, R01 NS036736, R01 NS043802-05, R01 NS043802, R01 NS045048-05, R01 NS044178-05] Funding Source: Medline
Calpain is a ubiquitous calcium-sensitive protease that is essential for normal physiologic neuronal function. However, alterations in calcium homeostasis lead to persistent, pathologic activation of calpain in a number of neurodegenerative diseases. Pathologic activation of calpain results in the cleavage of a number of neuronal substrates that negatively affect neuronal structure and function, leading to inhibition of essential neuronal survival mechanisms. In this review, we examine the mechanistic underpinnings of calcium dysregulation resulting in calpain activation in the acute neurodegenerative diseases such as cerebral ischemia and in the chronic neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, Huntington's disease, multiple sclerosis, prion-related encephalopathy, and amylotrophic lateral sclerosis. The premise of this paper is that analysis of the signaling and transcriptional consequences of calpain-mediated cleavage of its various substrates for any neurodegenerative disease can be extrapolated to all of the neurodegenerative diseases vulnerable to calcium dysregulation.
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