Abstract：
Alzheimer\'s disease (AD) is a fatal neurodegenerative disease in which senile plaques and neurofibrillary tangles are crucially involved in its physiological and pathophysiological processes. Growing animal and clinical studies have suggested that AD is also comorbid with some metabolic diseases, including type 2 diabetes mellitus (T2DM), and therefore, it is often considered brain diabetes. AD and T2DM share multiple molecular and biochemical mechanisms, including impaired insulin signaling, oxidative stress, gut microbiota dysbiosis, and mitochondrial dysfunction. In this review article, we mainly introduce oxidative stress and mitochondrial dysfunction and explain their role and the underlying molecular mechanism in T2DM and AD pathogenesis; then, according to the current literature, we comprehensively evaluate the possibility of regulating oxidative homeostasis and mitochondrial function as therapeutics against AD. Furthermore, considering dietary polyphenols\' antioxidative and antidiabetic properties, the strategies for applying them as potential therapeutical interventions in patients with AD symptoms are assessed.
摘要：
阿尔茨海默病(Alzheimer’sdisease,AD)是一种致命性的神经退行性疾病,其中老年斑和神经原纤维缠结在其生理和病理生理过程中起着至关重要的作用。越来越多的动物和临床研究表明，AD也与一些代谢性疾病并存，包括2型糖尿病（T2DM），因此,它通常被认为是脑型糖尿病。AD和T2DM具有多种分子和生化机制，包括受损的胰岛素信号，氧化应激，肠道菌群失调，和线粒体功能障碍。在这篇评论文章中，主要介绍氧化应激和线粒体功能障碍,阐述其在T2DM和AD发病机制中的作用和潜在的分子机制;根据目前的文献,我们全面评估了调节氧化稳态和线粒体功能作为治疗AD的可能性。此外，考虑到膳食多酚的抗氧化和抗糖尿病特性，评估了将其作为AD症状患者的潜在治疗干预措施的策略.
