组织蛋白酶
神经退行性变
老年斑
阿尔茨海默病
蛋白酵素
组织蛋白酶B
发病机制
组织蛋白酶D
自噬
医学
生物
疾病
免疫学
病理
生物化学
细胞凋亡
酶
作者
Azizul Haque,Naren L. Banik,Swapan K. Ray
出处
期刊:Cns & Neurological Disorders-drug Targets
[Bentham Science]
日期:2008-06-01
卷期号:7 (3): 270-277
被引量:49
标识
DOI:10.2174/187152708784936653
摘要
Endolysosomal proteases such as cysteinyl and aspartyl cathepsins play diverse roles in inflammatory autoimmune diseases, cancers, and neurodegenerative diseases. Cysteinyl cathepsin B and aspartyl cathepsin D levels are markedly elevated in a variety of neurological disorders including Alzheimers disease (AD), a leading cause of dementia in the elderly. Studies have also shown an increased cathepsin activity in AD patients where senile plaques and neuronal loss are marked features of the disease. Senile plaques contain amyloid-beta (Aβ) peptide, which is produced by proteolytic cleavage of the amyloid precursor protein (APP) by the proteases. In this article, we present the current knowledge of cysteinyl and aspartyl cathepsins in cellular and molecular events that lead to formation of senile plaques in AD. This article also focused on the role of cathepsin inhibitors as disease-modifying treatment strategies that could halt, or even prevent, this devastating neurological disorder. Keywords: Cathepsins, amyloid-beta (Aβ) peptide, immune responses, autophagy, neurodegeneration, apoptosis, Alzheimer's disease (AD), cathepsin inhibitors
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