Department of Chemistry, Centre of Membrane Sciences, and Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY 40506-0055, USA.
J Alzheimers Dis. 2011;24(1):77-84. doi: 10.3233/JAD-2011-101425.
Alzheimer's disease (AD) is histopathologically characterized by the presence of senile plaques, neurofibrillary tangles, and synapse loss. The main component of senile plaques is amyloid β-peptide (Aβ), which has been shown to induce oxidative stress in in vitro and in vivo studies. AD is associated with elevated levels of oxidative damage in brain and peripheral lymphocytes. Further Aβ has been found to be accumulated in mitochondria, which might contribute to the reported alterations in the mitochondrial morphology, and impaired mitochondrial energy metabolism in AD brain. Biomarkers are desperately needed for earlier diagnosis of AD and to monitor efficacy of new therapies. Hence, in the present study we show that markers of oxidative damage are elevated in mitochondria isolated from AD lymphocytes suggesting that these oxidative stress indices potentially could serve as a viable biomarker for AD.
阿尔茨海默病（AD）在组织病理学上的特征是存在老年斑、神经纤维缠结和突触丧失。老年斑的主要成分是β淀粉样肽（Aβ），体外和体内研究表明 Aβ 可诱导氧化应激。AD 与大脑和外周淋巴细胞中氧化损伤水平升高有关。进一步的研究发现 Aβ 在 线粒体中积累，这可能导致 AD 大脑中线粒体形态的改变和线粒体能量代谢受损。因此，在本研究中我们发现，从 AD 淋巴细胞中分离出的线粒体中的氧化损伤标志物升高，这表明这些氧化应激指标可能成为 AD 的可行生物标志物。
