氧化应激
路易氏体型失智症
疾病
共核细胞病
脂质过氧化
蛋白质聚集
痴呆
化学
炎症
淀粉样蛋白(真菌学)
帕金森病
医学
神经科学
生物化学
α-突触核蛋白
生物
病理
内科学
作者
Jan Bieschke,Qinghai Zhang,Daryl A. Bosco,Richard A. Lerner,Evan T. Powers,Paul Wentworth,Jeffery W. Kelly
摘要
Oxidative stress and inflammation are risk factors for both the development of alpha-synucleinopathies, such as Parkinson's disease and dementia with Lewy bodies, and Alzheimer's disease, the two most common neurodegenerative disorders. These diseases are associated with the neurotoxic deposition of misassembled alpha-synuclein and amyloid-beta (Abeta) peptides, respectively. Both occur sporadically, that is, without detectable disease-related mutations, in the vast majority of cases. Small molecule oxidation products, especially secosterols derived from cholesterol and 4-hydroxynonenal derived from lipid peroxidation, found in afflicted brains, accelerate the misassembly of both Abeta and alpha-synuclein. This Account explores the mechanism of small molecule oxidation product-mediated protein misassembly and possible intervention strategies.
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