氧化应激
亨廷顿蛋白
高磷酸化
发病机制
神经毒性
活性氧
神经退行性变
蛋白质聚集
氧化磷酸化
生物
淀粉样蛋白(真菌学)
细胞生物学
化学
生物化学
医学
毒性
突变体
免疫学
疾病
病理
基因
激酶
有机化学
植物
出处
期刊:Revista medico-chirurgicală̆ a Societă̆ţ̜ii de Medici ş̧i Naturaliş̧ti din Iaş̧i
[Grigore T. Popa University of Medicine and Pharmacy]
日期:2014-01-01
卷期号:118 (1): 19-27
被引量:18
摘要
Protein aggregates are the defining pathological feature of human neurodegenerative diseases. Studies have revealed that mutant huntingtin, polyglutamine-expanded ataxin-1 and ataxin-3 can cause elevated levels of reactive oxygen species in neuronal cells. It has also been indicated that the normal host prion protein behaves as an antioxidant, while the neurotoxic peptide based on the sequence of the scrapie isoform increases hydrogen peroxide toxicity in neuronal cultures. Additionally, not only can oxidative stress contribute to the aggregation of beta-amyloid and alpha-synuclein, but both beta-amyloid and alpha-synuclein can induce oxidative damage. Furthermore, oxidative stressors have been shown to play a critical role in neurofibrillary pathology leading to tau hyperphosphorylation. In conclusion, the present review supports a cause-effect relationship between oxidative stress and toxic proteins in the pathogenesis of neurodegenerative disorders.
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