Institute of Medical Biochemistry Leopoldo de Meis, Federal University of Rio de Janeiro, Rio de Janeiro, RJ 21941-902, Brazil; Institute of Biophysics Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, RJ 21941-902, Brazil.
Institute of Medical Biochemistry Leopoldo de Meis, Federal University of Rio de Janeiro, Rio de Janeiro, RJ 21941-902, Brazil.
Neuropharmacology. 2018 Jul 1;136(Pt B):160-171. doi: 10.1016/j.neuropharm.2017.11.014. Epub 2017 Nov 10.
Alzheimer's disease (AD) is a risk factor for type 2 diabetes and vice versa, and a growing body of evidence indicates that these diseases are connected both at epidemiological, clinical and molecular levels. Recent studies have begun to reveal common pathogenic mechanisms shared by AD and type 2 diabetes. Impaired neuronal insulin signaling and endoplasmic reticulum (ER) stress are present in animal models of AD, similar to observations in peripheral tissue in T2D. These findings shed light into novel diabetes-related mechanisms leading to brain dysfunction in AD. Here, we review the literature on selected mechanisms shared between these diseases and discuss how the identification of such mechanisms may lead to novel therapeutic targets in AD. This article is part of the Special Issue entitled 'Metabolic Impairment as Risk Factors for Neurodegenerative Disorders.'
阿尔茨海默病(AD)是 2 型糖尿病的一个风险因素,反之亦然,越来越多的证据表明这两种疾病在流行病学、临床和分子水平上相互关联。最近的研究开始揭示 AD 和 2 型糖尿病共有的常见致病机制。在 AD 的动物模型中存在神经元胰岛素信号和内质网(ER)应激,这与 T2D 外周组织中的观察结果相似。这些发现为 AD 中导致脑功能障碍的新型糖尿病相关机制提供了线索。在这里,我们回顾了这些疾病之间共享的一些选定机制的文献,并讨论了如何确定这些机制可能为 AD 带来新的治疗靶点。本文是主题为“代谢障碍作为神经退行性疾病的风险因素”的特刊的一部分。