Alterations in diabetes mellitus gene expression in the development and progression of Alzheimer’s disease: The PI3K/Akt pathway link

IF 0.5 Q4 CLINICAL NEUROLOGY Revista Mexicana de Neurociencia Pub Date : 2021-10-11 DOI:10.24875/rmn.20000087
Karla Aketzalli Hernández-Contreras, M. Hernández-Aguilar, D. Herrera-Covarrubias, F. Rojas-Durán, G. Aranda-Abreu
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Abstract

Considered a neurodegenerative disease, Alzheimer’s disease (AD) involves a physiopathological process characterized by the presence of the beta-amyloid peptide, hyperphosphorylated Tau protein, and neuroinflammation. Diabetes mellitus (DM) is an endocrine disease characterized by insulin resistance, where decreased production of this hormone causes a constant state of hyperglycemia. Although it is recognized that DM is a risk factor for the development of AD, the compression of the mechanisms involved is not completely understood. The present review evaluates the information acquired from primary and secondary sources, focusing on the alterations in gene expression associated with AD as well as the alterations in gene expression associated with DM, to later highlight the influence that these types of alterations developed in patients with DM can have on both the development and progression of AD. Finally, we point out those alterations that impact the phospha-tidyl Inositol 3 Kinase/Akt (PI3K/Akt) pathway, which seems to intervene in the physiopathological process of both diseases, considering that the compression of these gene alterations can help us understand the intricate link between DM and AD.
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糖尿病基因表达在阿尔茨海默病发生和进展中的改变:PI3K/Akt通路的联系
阿尔茨海默病(AD)被认为是一种神经退行性疾病,涉及一个以β淀粉样肽、过度磷酸化Tau蛋白和神经炎症为特征的生理病理过程。糖尿病(DM)是一种以胰岛素抵抗为特征的内分泌疾病,这种激素的产生减少会导致持续的高血糖状态。尽管人们已经认识到糖尿病是AD发展的风险因素,但对相关机制的压缩还不完全清楚。本综述评估了从一级和二级来源获得的信息,重点关注与AD相关的基因表达的改变以及与DM相关的基因表现的改变,以强调DM患者发生的这些类型的改变可能对AD的发展和进展产生的影响。最后,我们指出了那些影响磷脂酰肌醇3激酶/Akt(PI3K/Akt)途径的改变,该途径似乎干预了这两种疾病的生理病理过程,考虑到这些基因改变的压缩可以帮助我们理解糖尿病和AD之间的复杂联系。
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来源期刊
Revista Mexicana de Neurociencia
Revista Mexicana de Neurociencia CLINICAL NEUROLOGY-
自引率
0.00%
发文量
28
审稿时长
28 weeks
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