De Sousa Ricardo Augusto Leoni
School of Biological Sciences and Health, Physical Education Department, Universidade Federal Dos Vales Do Jequitinhonha E Mucuri, Diamantina, Minas Gerais, Brazil.
Multicenter Post Graduation Program in Physiological Sciences (PMPGCF), Brazilian Society of Physiology, São Paulo, Brazil.
Metab Brain Dis. 2022 Apr;37(4):851-857. doi: 10.1007/s11011-022-00953-2. Epub 2022 Mar 14.
Alzheimer's disease (AD) is a neurodegenerative disorder that leads to cognitive decline and memory loss. Insulin resistance in central nervous system (CNS) is a common feature in dementia. Defective insulin signaling is associated to higher levels of inflammation and to neuronal dysfunction. A reactive gliosis, a change that occurs in glial cells due to damage in CNS, seems to be one of the most important pro-inflammatory mechanisms in AD pathology. The first response to CNS injury is the migration of macrophages and microglia to the specific site of the injury. Oligodendrocytes are also recruited to to contribute with remyelination. The last component of a reactive gliosis is astrogliosis, which is the enhancement of astrocytes expression with concomitant changes in its morphology being the main cells of the glial scar. Here, we review the mechanisms by which a reactive gliosis can induce or contribute to the development and progression of AD.
阿尔茨海默病（AD）是一种导致认知衰退和记忆丧失的神经退行性疾病。中枢神经系统（CNS）中的胰岛素抵抗是痴呆症的一个常见特征。胰岛素信号缺陷与更高水平的炎症和神经元功能障碍有关。反应性胶质增生是由于中枢神经系统损伤而在胶质细胞中发生的一种变化，似乎是AD病理学中最重要的促炎机制之一。对中枢神经系统损伤的第一反应是巨噬细胞和小胶质细胞迁移到损伤的特定部位。少突胶质细胞也被招募来参与髓鞘再生。反应性胶质增生的最后一个组成部分是星形胶质细胞增生，即星形胶质细胞表达增强，同时其形态发生变化，成为胶质瘢痕的主要细胞。在此，我们综述反应性胶质增生可诱导或促进AD发生和发展的机制。
