Lovell Mark A, Markesbery William R
Department of Chemistry, University of Kentucky, Lexington, Kentucky, USA.
J Neurosci Res. 2007 Nov 1;85(14):3036-40. doi: 10.1002/jnr.21346.
Increasing evidence supports a role for oxidative damage in the pathogenesis of Alzheimer's disease (AD). Multiple studies show significantly increased levels of lipid peroxidation and protein, DNA, and RNA oxidation in vulnerable regions of the brain of patients with late-stage AD (LAD). More recent studies of patients with amnestic mild cognitive impairment (MCI), the earliest clinical manifestation of AD, show similar patterns of oxidative damage. These observations suggest that oxidative damage to critical biomolecules occurs early in the pathogenesis of AD and precedes pronounced neuropathologic alterations. Because oxidative damage begins early in the progress of the disease, it represents a potential therapeutic target for slowing the onset and progression of AD.
越来越多的证据支持氧化损伤在阿尔茨海默病(AD)发病机制中起作用。多项研究表明,晚期AD(LAD)患者大脑易损区域的脂质过氧化以及蛋白质、DNA和RNA氧化水平显著升高。对AD最早临床表现——遗忘型轻度认知障碍(MCI)患者的最新研究显示,氧化损伤模式相似。这些观察结果表明,关键生物分子的氧化损伤在AD发病机制中出现较早,且先于明显的神经病理改变。由于氧化损伤在疾病进展早期就已开始,它代表了一个减缓AD发病和进展的潜在治疗靶点。