Rosales-Corral Sergio, Tan Dun-Xian, Manchester Lucien, Reiter Russel J
Centro de Investigación Biomédica de Occidente, Instituto Mexicano del Seguro Social, Sierra Mojada 800, Colonia Independencia, 44340 Guadalajara, JAL, Mexico.
Department of Structural Biology, The University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229-3900, USA.
Oxid Med Cell Longev. 2015;2015:985845. doi: 10.1155/2015/985845. Epub 2015 Feb 26.
There are several oxidative stress-related pathways interconnecting Alzheimer's disease and type II diabetes, two public health problems worldwide. Coincidences are so compelling that it is attractive to speculate they are the same disorder. However, some pathological mechanisms as observed in diabetes are not necessarily the same mechanisms related to Alzheimer's or the only ones related to Alzheimer's pathology. Oxidative stress is inherent to Alzheimer's and feeds a vicious cycle with other key pathological features, such as inflammation and Ca(2+) dysregulation. Alzheimer's pathology by itself may lead to insulin resistance in brain, insulin resistance being an intervening variable in the neurodegenerative disorder. Hyperglycemia and insulin resistance from diabetes, overlapping with the Alzheimer's pathology, aggravate the progression of the neurodegenerative processes, indeed. But the same pathophysiological background is behind the consequences, oxidative stress. We emphasize oxidative stress and its detrimental role in some key regulatory enzymes.
在全球范围内，有几种与氧化应激相关的途径将阿尔茨海默病和II型糖尿病这两个公共卫生问题联系起来。两者之间的巧合非常明显，以至于人们很容易推测它们是同一种疾病。然而，糖尿病中观察到的一些病理机制不一定与阿尔茨海默病相关的机制相同，也不一定是与阿尔茨海默病病理相关的唯一机制。氧化应激是阿尔茨海默病所固有的，并与其他关键病理特征（如炎症和钙（Ca2+）调节异常）形成恶性循环。阿尔茨海默病本身可能导致大脑中的胰岛素抵抗，而胰岛素抵抗是神经退行性疾病中的一个中间变量。事实上，糖尿病引起的高血糖和胰岛素抵抗与阿尔茨海默病病理重叠，加剧了神经退行性过程的进展。但这些后果背后有着相同的病理生理背景，即氧化应激。我们强调氧化应激及其在一些关键调节酶中的有害作用。
