脑啡肽酶
胰岛素降解酶
氧化应激
蛋白质水解
神经退行性变
淀粉样蛋白(真菌学)
蛋白酵素
淀粉样前体蛋白
老化
生物化学
酶
化学
阿尔茨海默病
生物
内科学
医学
疾病
无机化学
作者
Natalia N. Nalivaeva,Anthony J. Turner
出处
期刊:Current Aging Science
[Bentham Science]
日期:2016-12-02
卷期号:10 (1): 32-40
被引量:31
标识
DOI:10.2174/1874609809666161111101111
摘要
The accumulation of cerebral amyloid β-peptide (Aβ) is a key precipitating factor for neuronal cell death in Alzheimer's Disease (AD). However, brain Aβ levels are modifiable since there is a balance between its formation from the Amyloid Precursor Protein (APP) and its removal by clearance mechanisms, which can be either through proteolysis or by protein binding and subsequent transport). Among the major enzymes degrading brain Aβ are several zinc-proteases: neprilysin (NEP), its homologues NEP2 and the Endothelin Converting Enzymes (ECE-1 and -2) and also the Insulin-Degrading Enzyme (IDE). During the ageing process, and under certain pathological conditions (e.g. ischemia and stroke), the expression and activity of these enzymes decline, which leads to a deficit of Aβ clearance and its accumulation in the brain. Some of these changes in the enzyme properties are due to their reduced expression and/or structural modification by reactive oxygen species. In this review paper we shall discuss some mechanisms of regulation of Amyloid-Degrading Enzymes (ADEs) and possible therapeutic approaches which might prevent their decline with age and after pathology. Keywords: Ageing, Alzheimer's disease, amyloid clearance, amyloid-degrading enzymes, neprilysin, oxidative stress, proteolysis.
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