Microglia, the primary immune cells in the central nervous system (CNS), play a critical role in maintaining CNS homeostasis through neurogenesis, synaptic pruning, and immune responses. In autism spectrum disorder (ASD), microglial dysfunction is increasingly recognized as a key contributor to neurodevelopmental abnormalities. Microglia are involved in synaptic pruning during early development, and their abnormal activation can lead to impaired synaptic function, neuroinflammation, and behavioral deficits. ASD is a heterogeneous neurodevelopmental disorder influenced by genetic and environmental factors, with microglial abnormalities potentially contributing to the pathogenesis of ASD. Studies have shown that microglia regulate neurogenesis and synaptic pruning, and their dysfunction can lead to altered brain development, including abnormal synaptic connectivity and impaired neuronal function. Microglial activation is associated with increased levels of pro-inflammatory cytokines such as TNF-α, which can disrupt synaptic pruning and neurogenesis. Additionally, microglia interact with other CNS cells, including neurons, astrocytes, and oligodendrocytes, to regulate brain development and function. Abnormal microglial activity, such as excessive phagocytosis or impaired synaptic pruning, can lead to neuroinflammation and altered neural circuits, contributing to ASD-like behaviors. The role of microglia in ASD is complex, involving multiple signaling pathways, including the complement cascade, PI3K/AKT, and MAPK pathways. Targeting microglial activation or dysfunction may offer new therapeutic strategies for ASD. Understanding the mechanisms by which microglia influence neurodevelopment and brain function in ASD is crucial for developing effective interventions.Microglia, the primary immune cells in the central nervous system (CNS), play a critical role in maintaining CNS homeostasis through neurogenesis, synaptic pruning, and immune responses. In autism spectrum disorder (ASD), microglial dysfunction is increasingly recognized as a key contributor to neurodevelopmental abnormalities. Microglia are involved in synaptic pruning during early development, and their abnormal activation can lead to impaired synaptic function, neuroinflammation, and behavioral deficits. ASD is a heterogeneous neurodevelopmental disorder influenced by genetic and environmental factors, with microglial abnormalities potentially contributing to the pathogenesis of ASD. Studies have shown that microglia regulate neurogenesis and synaptic pruning, and their dysfunction can lead to altered brain development, including abnormal synaptic connectivity and impaired neuronal function. Microglial activation is associated with increased levels of pro-inflammatory cytokines such as TNF-α, which can disrupt synaptic pruning and neurogenesis. Additionally, microglia interact with other CNS cells, including neurons, astrocytes, and oligodendrocytes, to regulate brain development and function. Abnormal microglial activity, such as excessive phagocytosis or impaired synaptic pruning, can lead to neuroinflammation and altered neural circuits, contributing to ASD-like behaviors. The role of microglia in ASD is complex, involving multiple signaling pathways, including the complement cascade, PI3K/AKT, and MAPK pathways. Targeting microglial activation or dysfunction may offer new therapeutic strategies for ASD. Understanding the mechanisms by which microglia influence neurodevelopment and brain function in ASD is crucial for developing effective interventions.