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脑葡萄糖转运蛋白:在阿尔茨海默病发病机制中的作用及潜在治疗靶点。

Brain Glucose Transporters: Role in Pathogenesis and Potential Targets for the Treatment of Alzheimer's Disease.

机构信息

Chair and Department of General Biology and Parasitology, Medical University of Warsaw, 5 Chalubinskiego Str., 02-004 Warsaw, Poland.

出版信息

Int J Mol Sci. 2021 Jul 29;22(15):8142. doi: 10.3390/ijms22158142.

DOI:10.3390/ijms22158142
PMID:34360906
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8348194/
Abstract

The most common cause of dementia, especially in elderly people, is Alzheimer's disease (AD), with aging as its main risk factor. AD is a multifactorial neurodegenerative disease. There are several factors increasing the risk of AD development. One of the main features of Alzheimer's disease is impairment of brain energy. Hypometabolism caused by decreased glucose uptake is observed in specific areas of the AD-affected brain. Therefore, glucose hypometabolism and energy deficit are hallmarks of AD. There are several hypotheses that explain the role of glucose hypometabolism in AD, but data available on this subject are poor. Reduced transport of glucose into neurons may be related to decreased expression of glucose transporters in neurons and glia. On the other hand, glucose transporters may play a role as potential targets for the treatment of AD. Compounds such as antidiabetic drugs, agonists of SGLT1, insulin, siRNA and liposomes are suggested as therapeutics. Nevertheless, the suggested targets of therapy need further investigations.

摘要

痴呆症最常见的病因,尤其是在老年人中,是阿尔茨海默病(AD),其主要危险因素是衰老。AD 是一种多因素神经退行性疾病。有几个因素会增加 AD 发展的风险。阿尔茨海默病的主要特征之一是大脑能量受损。在受 AD 影响的大脑的特定区域观察到葡萄糖摄取减少引起的代谢低下。因此,葡萄糖代谢低下和能量不足是 AD 的标志。有几个假说解释了葡萄糖代谢低下在 AD 中的作用,但关于这个主题的数据很少。葡萄糖进入神经元的转运减少可能与神经元和神经胶质中葡萄糖转运体表达减少有关。另一方面,葡萄糖转运体可能作为 AD 治疗的潜在靶点发挥作用。抗糖尿病药物、SGLT1 激动剂、胰岛素、siRNA 和脂质体等化合物被建议作为治疗药物。然而,治疗的建议靶点需要进一步研究。

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