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膳食多酚通过 PI3K/Akt 信号通路在 2 型糖尿病与阿尔茨海默病的相互作用中改善氧化应激和线粒体功能障碍的作用。

The roles of dietary polyphenols at crosstalk between type 2 diabetes and Alzheimer's disease in ameliorating oxidative stress and mitochondrial dysfunction via PI3K/Akt signaling pathways.

机构信息

Food Science and Technology Program, Department of Life Sciences, BNU-HKBU United International College, Zhuhai, Guangdong 519087, China; Centre for Cancer and Inflammation Research, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong, China.

Food Science and Technology Program, Department of Life Sciences, BNU-HKBU United International College, Zhuhai, Guangdong 519087, China.

出版信息

Ageing Res Rev. 2024 Aug;99:102416. doi: 10.1016/j.arr.2024.102416. Epub 2024 Jul 13.

DOI:10.1016/j.arr.2024.102416
PMID:39002644
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(AD)是一种致命的神经退行性疾病,其生理和病理生理过程中涉及到老年斑和神经原纤维缠结。越来越多的动物和临床研究表明,AD 还与一些代谢疾病共病,包括 2 型糖尿病(T2DM),因此,它通常被认为是“大脑糖尿病”。AD 和 T2DM 具有多种分子和生化机制,包括胰岛素信号受损、氧化应激、肠道微生物失调和线粒体功能障碍。在这篇综述文章中,我们主要介绍氧化应激和线粒体功能障碍,并解释它们在 T2DM 和 AD 发病机制中的作用及其潜在的分子机制;然后,根据目前的文献,我们全面评估了调节氧化平衡和线粒体功能作为治疗 AD 的可能性。此外,鉴于膳食多酚的抗氧化和抗糖尿病特性,评估了将它们作为治疗 AD 症状患者的潜在治疗干预措施的策略。

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