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痴呆的细胞和分子机制:解析糖尿病与阿尔茨海默病之间的因果关联。

Cellular and Molecular Mechanisms of Dementia: Decoding the Causal link of Diabetes Mellitus in Alzheimer's Disease.

机构信息

Center of Excellence in Genomic Medicine Research, Faculty of Applied Medical Sciences, King Abdulaziz University, Jeddah, Saudi Arabia.

Institute of Molecular Biology & Biotechnology (IMBB), the University of Lahore, Lahore, Pakistan.

出版信息

CNS Neurol Disord Drug Targets. 2021;20(7):602-612. doi: 10.2174/1871527320666210212114116.

Abstract

Dementia and diabetes are the two major disorders that are linked at both biochemical and molecular levels, which is due to the existing similarities between pancreatic beta-cells and neuronal cells at the transcriptional and translational levels. Both diseases have similar causative genes or factors, and dementia is one of the advanced complications in about 50-52% of patients with Type 2 Diabetes Mellitus (T2DM). Further, patients with T2DM are at a higher risk of neuronal degeneration and Alzheimer's Disease (AD). Dementia, which is most common in AD, is associated with diminished insulin receptors by nearly 80%. The impairment in insulin signaling thus leads to the development of dementia and AD. Biochemical changes in 'tau' protein and amyloid-- beta proteins make them critical players in the formation of plaques in patients with dementia and AD. Here, we decode various cellular and molecular mechanisms associated with the development of dementia in patients with diabetes and AD.

摘要

痴呆症和糖尿病是两种主要的疾病,它们在生化和分子水平上相互关联,这是由于胰腺β细胞和神经元细胞在转录和翻译水平上存在相似性。这两种疾病有相似的致病基因或因素,痴呆症是大约 50-52%的 2 型糖尿病(T2DM)患者的晚期并发症之一。此外,T2DM 患者更容易出现神经元退化和阿尔茨海默病(AD)。在 AD 中最常见的痴呆症,其胰岛素受体减少了近 80%。胰岛素信号的损伤导致了痴呆症和 AD 的发生。'tau'蛋白和淀粉样-β蛋白的生化变化使它们成为痴呆症和 AD 患者斑块形成的关键因素。在这里,我们解码了与糖尿病和 AD 患者痴呆症发展相关的各种细胞和分子机制。

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