Faculty of Military Health Sciences, University of Defence, Trebesska 1575, 50001 Hradec Kralove, Czech Republic.
Curr Med Chem. 2014;21(3):356-64. doi: 10.2174/09298673113206660258.
Alzheimer´s disease (AD) is a neurodegenerative disorder with no known cure and rapid rise in incidence. The predominant cognitive impairment is currently treated using cognitive enhancers like cholinesterase inhibitors. The two molecular hallmarks of AD are amyloid plaques created from an amyloid precursor protein and hyperphosphorylated tau protein that is deposited as neurofibrillary tangles inside neurons. A number of pathological mechanisms follow or precede these formations. Alteration in mitochondrial function and deposition of heavy metals are reported. The disease progression is enhanced by oxidative stress. However, the role of oxidative stress is not universally accepted. The current review covers and discusses the basic evidence and role of oxidative stress in AD development.
阿尔茨海默病（AD）是一种神经退行性疾病，目前尚无已知的治愈方法，且发病率迅速上升。目前主要采用胆碱酯酶抑制剂等认知增强剂来治疗主要的认知障碍。AD 的两个主要分子特征是由淀粉样前体蛋白产生的淀粉样斑块和过度磷酸化的 tau 蛋白，这些蛋白沉积在神经元内形成神经原纤维缠结。许多病理机制紧随这些形成物出现或先于这些形成物出现。据报道，线粒体功能的改变和重金属的沉积。氧化应激会加速疾病的进展。然而，氧化应激的作用并非被普遍接受。本综述涵盖并讨论了氧化应激在 AD 发展中的基本证据和作用。
