TY -的A2锣Cheng-Xin AU -肯尼,葆拉·m . AU -贝内特,James p . PY - 2019 DA - 2019/03/05 TI -阿尔茨海默病额叶皮层线粒体显示个人呼吸蛋白的损失但保护呼吸道Supercomplexes SP - 4814783六世- 2019 AB -阿尔茨海默病(AD),老年痴呆症是导致成人偶发性痴呆的最常见原因，随着年龄的增长，其发生的风险增加，并注定在未来几十年成为一个重大的社会医疗悲剧。虽然其起源可能复杂，但散发性AD的特点是进行性和定型的神经病理，伴有聚集蛋白沉积(尤其是β淀粉样蛋白(BA)和过度磷酸化tau蛋白(P-tau))和神经元变性。迄今为止，预防BA的合成或免疫介导的BA去除都未能改变AD的进展。P-tau疗法的开发和测试工作正在进行中。AD的脑组织显示多种系统缺陷，包括呼吸能力丧失。在本研究中，AD和CTL样本的线粒体质量没有差异。我们通过Western免疫印迹法检测了死后AD和CTL额叶皮质的线粒体制备，以了解单个呼吸蛋白复合物的相对水平。方差分析显示AD患者所有呼吸复合体亚单位均存在缺陷;方差分析后t检验显示复合物II、III和V的亚单位水平存在显著差异，复合物IV亚单位的边缘显著性。 and no difference for subunit of complex I. We also examined mitochondrial extracts with blue-native gel electrophoresis combined with immunoblotting for subunits of complexes I and III to search for “respiratory supercomplexes” (RSC’s). We found that levels of RSC’s did not differ between AD and CTL samples. Mitochondrial preparations from end-stage AD brain tissue showed loss of individual ATP-producing respiration subunits but preservation of levels of assembled respiratory subunits into RSC’s. Possible explanations include insufficient sensitivity of our method of RSC detection to find loss of individual subunits, or normal levels of RSC’s in AD brain mitochondria coupled with decreased levels of nonassembled respiratory complex subunits. Disease-altering therapies of early AD could include stimulation of mitochondrial biogenesis to overcome loss of respiratory subunits. SN - 2090-8024 UR - https://doi.org/10.1155/2019/4814783 DO - 10.1155/2019/4814783 JF - International Journal of Alzheimer’s Disease PB - Hindawi KW - ER -