Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China.
CNS Neurosci Ther. 2023 Jun;29 Suppl 1(Suppl 1):59-73. doi: 10.1111/cns.14077. Epub 2023 Jan 4.
Diabetic cognitive dysfunction (DCD) is one of the most insidious complications of type 2 diabetes mellitus, which can seriously affect the ability to self-monitoring of blood glucose and the quality of life in the elderly. Previous pathological studies of cognitive dysfunction have focused on neuronal dysfunction, characterized by extracellular beta-amyloid deposition and intracellular tau hyperphosphorylation. In recent years, astrocytes have been recognized as a potential therapeutic target for cognitive dysfunction and important participants in the central control of metabolism. The disorder of gut microbiota and their metabolites have been linked to a series of metabolic diseases such as diabetes mellitus. The imbalance of intestinal flora has the effect of promoting the occurrence and deterioration of several diabetes-related complications. Gut microbes and their metabolites can drive astrocyte activation.
We reviewed the pathological progress of DCD related to the "gut microbiota-astrocyte" axis in terms of peripheral and central inflammation, intestinal and blood-brain barrier (BBB) dysfunction, systemic and brain energy metabolism disorders to deepen the pathological research progress of DCD and explore the potential therapeutic targets.
"Gut microbiota-astrocyte" axis, unique bidirectional crosstalk in the brain-gut axis, mediates the intermediate pathological process of neurocognitive dysfunction secondary to metabolic disorders in diabetes mellitus.
糖尿病认知功能障碍(DCD)是 2 型糖尿病最隐匿的并发症之一,可严重影响老年患者的自我血糖监测能力和生活质量。既往认知功能障碍的病理学研究主要集中在神经元功能障碍上,其特征是细胞外β-淀粉样蛋白沉积和细胞内 tau 过度磷酸化。近年来,星形胶质细胞已被认为是认知功能障碍的潜在治疗靶点,也是代谢调控的重要参与者。肠道微生物群及其代谢物的紊乱与一系列代谢性疾病如糖尿病有关。肠道菌群失衡具有促进多种与糖尿病相关并发症发生和恶化的作用。肠道微生物及其代谢产物可以驱动星形胶质细胞的激活。
我们从外周和中枢炎症、肠道和血脑屏障(BBB)功能障碍、全身和脑能量代谢紊乱等方面综述了与“肠道微生物群-星形胶质细胞”轴相关的 DCD 的病理进展,以深化 DCD 的病理研究进展,并探讨潜在的治疗靶点。
“肠道微生物群-星形胶质细胞”轴作为脑肠轴中独特的双向交流,介导了糖尿病代谢紊乱导致的神经认知功能障碍的中间病理过程。