Roles of the Notch signaling pathway and microglia in autism.

This review looks at how two biological processes - the Notch signaling system and immune cells called microglia - might contribute to autism. The researchers suggest that when these systems don't work properly during brain development, it can lead to the learning, memory, and behavioral differences seen in autism. They propose that inflammation and problems with cellular cleanup processes may be involved.

This 2023 review examines the roles of Notch signaling pathway and microglia in autism pathogenesis. The authors propose that autism involves abnormal microglial increases in brain regions and disrupted Notch pathway activity. They discuss how Notch pathway dysfunction affects neuronal activities, leading to learning and memory impairments. The review suggests that increased microglial protein synthesis and abnormal autophagy impact synaptic development, contributing to behavioral abnormalities.

Additionally, they propose that Notch signaling regulates microglial activation and differentiation, promoting inflammatory responses. The interaction between excessive reactive oxygen species from microglia and impaired autophagy may further affect Notch signaling, potentially increasing autism susceptibility.

Findings suggest potential therapeutic targets through Notch pathway modulation or microglial regulation. However, translation to clinical practice requires substantial additional research. The proposed mechanisms are largely theoretical and need empirical validation before informing treatment approaches.

This is a narrative review without systematic methodology. No original data presented. Causal relationships between Notch signaling, microglia, and autism are largely theoretical. Limited discussion of contradictory evidence or alternative explanations for proposed mechanisms.

The Notch signaling pathway is mainly involved in the regulation of neural stem cell proliferation, survival and differentiation during the development of the central nervous system. As a neurodevelopmental disorder, autism is associated with an abnormal increase in the number of microglia in several brain regions. These findings suggest that the pathogenesis of autism may be related to the Notch signaling pathway and microglia. In this review, we discuss how Notch pathway activity leads to behavioral abnormalities such as learning and memory impairment by influencing neuronal biological activities.

An increase in microglial protein synthesis and abnormal autophagy can affect synaptic development and lead to behavioral abnormalities, and all of these changes can lead to autism. Furthermore, the Notch signaling pathway regulates the activation and differentiation of microglia and promotes inflammatory responses, leading to the occurrence of autism. When excessive reactive oxygen species (ROS) secreted by microglia cannot be cleared by autophagy in a timely manner, Notch signaling pathway activity is affected, possibly further increasing susceptibility to autism. This review reveals the mechanism underlying the role of the Notch signaling pathway, microglia and their interaction in the pathogenesis of autism and provides a theoretical reference for targeted clinical therapies for autism.