Aging and amyloid beta-induced oxidative DNA damage and mitochondrial dysfunction in Alzheimer's disease: implications for early intervention and therapeutics.
Aging and amyloid beta-induced oxidative DNA damage and mitochondrial dysfunction in Alzheimer's disease: implications for early intervention and therapeutics.
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DOI：
10.1016/j.bbadis.2011.08.005
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发表时间：
2011-11
影响因子：
6.2
通讯作者：
Reddy, P. Hemachandra
中科院分区：
文献类型：
--
作者：
Mao, Peizhong;Reddy, P. Hemachandra
阿尔茨海默病（AD）是一种与年龄相关的进行性神经退行性疾病，影响着世界上成千上万的人，并且仍然没有有效的治疗方法。二十多年来，使用 AD 死后大脑、转基因小鼠以及淀粉样前体蛋白和 tau 细胞模型进行的深入研究表明，β 淀粉样蛋白 (Aβ) 和过度磷酸化的 tau 蛋白协同参与触发疾病进展。越来越多的证据还表明，衰老和β淀粉样蛋白诱导的氧化DNA损伤和线粒体功能障碍会引发并促进该疾病的发生和进展。本文的目的是总结衰老和AD的最新进展，特别强调线粒体、氧化DNA损伤及其测量方法。它还讨论了氧化 DNA 损伤的治疗潜力和 AD 的治疗策略。
Alzheimer's disease (AD) is an age-related progressive neurodegenerative disease affecting thousands of people in the world and effective treatment is still not available. Over two decades of intense research using AD postmortem brains, transgenic mouse and cell models of amyloid precursor protein and tau revealed that amyloid beta (Aβ) and hyperphosphorylated tau are synergistically involved in triggering disease progression. Accumulating evidence also revealed that aging and amyloid beta-induced oxidative DNA damage and mitochondrial dysfunction initiates and contributes to the development and progression of the disease. The purpose of this article is to summarize the latest progress in aging and AD, with a special emphasis on the mitochondria, oxidative DNA damage including methods of its measurement. It also discusses the therapeutic potential of oxidative DNA damage and treatment strategies in AD.
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