Department of Chemistry, Center of Membrane Sciences, and Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY 40506-0055, USA.
J Alzheimers Dis. 2010;19(1):341-53. doi: 10.3233/JAD-2010-1222.
Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is characterized pathologically by the presence of senile plaques, neurofibrillary tangles, and synapse loss. Increasing evidence supports a role of amyloid beta-peptide (Abeta)-induced oxidative stress in the progression and pathogenesis of AD. In this review, we summarize evidence for a role of oxidative stress in the progression of AD by comparing the appearance of the same oxidized brain proteins from subjects with mild cognitive impairment (MCI), early AD (EAD), and late-stage AD, and relating these findings to the reported AD pathology. The identification of oxidized brain proteins in common in MCI, EAD, and AD brain suggest that certain key pathways are triggered and may be involved in the progression of AD. Exploring these pathways in detail may provide clues for better understanding the pathogenesis and progression of AD and also for the development of effective therapies to treat or delay this dementing disorder.
阿尔茨海默病（AD）是一种进行性神经退行性疾病，其病理特征为老年斑、神经纤维缠结和突触丧失。越来越多的证据支持淀粉样β肽（Abeta）诱导的氧化应激在 AD 的进展和发病机制中的作用。在这篇综述中，我们通过比较轻度认知障碍（MCI）、早期 AD（EAD）和晚期 AD 患者大脑中相同氧化脑蛋白的出现，总结了氧化应激在 AD 进展中的作用证据，并将这些发现与报告的 AD 病理学联系起来。在 MCI、EAD 和 AD 大脑中共同存在的氧化脑蛋白的鉴定表明，某些关键途径被触发，可能与 AD 的进展有关。详细研究这些途径可能为更好地理解 AD 的发病机制和进展提供线索，也为开发有效的治疗方法来治疗或延缓这种痴呆症提供线索。
