Involvement of IL-10R/STAT3 pathway in amyloid β clearance by microlgia in Alzheimer's disease

Both the total amount and annual growth rate of Alzheimer's disease (AD) patients in China are much higher than in other regions in the world. This trend of rapid growth will be difficult to change in the next few decades, hence the prevention and treatment situation of AD patients in China is more severe. Maintaining the balance between the production and removal pathways of A beta is an important guarantee for the body to maintain its normal physiological state. The dysfunction of A beta clearance is an important factor of A beta accumulation in brain tissue of AD patients causing neurotoxicity of synaptic damage and neuronal death. Based on the literature review, it introduced the important role of microglias in clearing A beta deposits in the process of Alzheimer's disease. And most of these phagocytic cells were the specific phenotype of disease-related microglia (DAM-I/DAM-II) that induced microglial differentiation after activation. IL-10KO promoted the transformation of microglial phenotype DAM-II, and enhanced its phagocytosis for A beta oligomers. There is a hypothesis that IL-10R/STAT3 negatively regulates microglial phagocytosis. It was learnt that blocking the IL-10R/STAT3 pathway promoted microglial activation and enhanced phagocytosis. The comprehensive review on the involvement of IL-10R/ STAT3 pathway in the process of AD would open up new ideas and discover new targets for the development of new therapeutic drugs.

Automated summary

The high number and growth rate of Alzheimer's disease patients in China pose challenges for prevention and treatment. Dysfunction in A β clearance is a key factor in AD development, with microglial cells playing an important role in clearing A β deposits. The IL-10R/STAT3 pathway may regulate microglial activation and phagocytosis, offering potential new targets for therapeutic drug development.