Markesbery William R, Lovell Mark A
Department of Neurology, University of Kentucky, Lexington, KY 40536-0230, USA.
Arch Neurol. 2007 Jul;64(7):954-6. doi: 10.1001/archneur.64.7.954.
Free radical-mediated oxidative damage is thought to play a role in the pathogenesis of Alzheimer disease. Previous studies have shown oxidative damage to lipids, proteins, DNA, and RNA in multiple brain regions in late-stage Alzheimer disease. Recent studies on patients with amnestic mild cognitive impairment who have undergone autopsy have shown increased lipid peroxidation as well as protein, DNA, and RNA oxidation in multiple brain regions. These studies establish oxidative damage as an early event in the pathogenesis of Alzheimer disease that can serve as a therapeutic target to slow the progression or perhaps the onset of the disease.
自由基介导的氧化损伤被认为在阿尔茨海默病的发病机制中起作用。先前的研究表明,在晚期阿尔茨海默病患者的多个脑区中,脂质、蛋白质、DNA和RNA均受到氧化损伤。最近对已接受尸检的遗忘型轻度认知障碍患者的研究表明,多个脑区的脂质过氧化以及蛋白质、DNA和RNA氧化均有所增加。这些研究证实氧化损伤是阿尔茨海默病发病机制中的早期事件,可作为减缓疾病进展或可能延缓疾病发作的治疗靶点。