Münch G, Thome J, Foley P, Schinzel R, Riederer P
Physiological Chemistry I, Theodor-Boveri-Institut (Biozentrum), Würzburg, Germany.
Brain Res Brain Res Rev. 1997 Feb;23(1-2):134-43. doi: 10.1016/s0165-0173(96)00016-1.
Accumulation of advanced glycation endproducts (AGE) in the brain is a feature of ageing and degeneration, especially in Alzheimer's disease (AD). Increased AGE levels explain many of the neuropathological and biochemical features of AD such as extensive protein crosslinking (beta-amyloid and MAP-tau), oxidative stress and neuronal cell death. Oxidative stress and AGEs initiate a positive feedback loop, where normal age-related changes develop into a pathophysiological cascade. Combined intervention using antioxidants, metal chelators, anti-inflammatory drugs and AGE-inhibitors may be a promising neuroprotective strategy.
晚期糖基化终末产物（AGE）在大脑中的积累是衰老和退化的一个特征，尤其是在阿尔茨海默病（AD）中。AGE水平升高解释了AD的许多神经病理学和生化特征，如广泛的蛋白质交联（β-淀粉样蛋白和微管相关蛋白tau）、氧化应激和神经元细胞死亡。氧化应激和AGEs引发一个正反馈循环，其中正常的与年龄相关的变化发展为病理生理级联反应。联合使用抗氧化剂、金属螯合剂、抗炎药物和AGE抑制剂进行干预可能是一种有前景的神经保护策略。
