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Potential key pathophysiological participant and treatment target in autism spectrum disorder: Microglia
Zehua Tan1, Ruixin Xia1, Xin Zhao1
1Department of Neurobiology, School of Basic Medicine, Fourth Military Medical University, Xi'an, Shaanxi 710032, China.
Abstract:
Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders characterized by social and communication deficits, as well as restricted or repetitive behaviors or interests. Although the etiology of ASD remains unclear, there is abundant evidence suggesting that microglial dysfunction is likely to be a significant factor in the pathophysiology of ASD. Microglia, the primary innate immune cells in the central nervous system (CNS), play a crucial role in brain development and homeostasis. Recently, numerous studies have shown that microglia in ASD models display various abnormalities including morphology, function, cellular interactions, genetic and epigenetic factors, as well as the expression of receptors, transcription factors, and cytokines. They impact normal neural development through various mechanisms contributing to ASD, such as neuroinflammation, and alterations in synaptic formation and pruning. The focus of this review is on recent studies regarding microglial abnormalities in ASD and their effects on the onset and progression of ASD at both cellular and molecular levels. It can provide insight into the specific contribution of microglia to ASD pathogenesis and help in designing potential therapeutic and preventative strategies targeting microglia.
Insights
Microglial dysfunction significantly contributes to autism spectrum disorder (ASD) pathogenesis by affecting neural development via neuroinflammation and altered synaptic processes. Understanding these microglial abnormalities offers potential therapeutic targets for ASD.
Area of Science:
- Neuroscience
- Immunology
- Developmental Biology
Background:
- Autism spectrum disorder (ASD) is a neurodevelopmental condition marked by social deficits and repetitive behaviors.
- The precise causes of ASD are unknown, but microglial dysfunction is increasingly implicated in its pathophysiology.
- Microglia, the brain's immune cells, are vital for neural development and homeostasis.
Purpose of the Study:
- To review recent research on microglial abnormalities in ASD models.
- To examine the impact of these abnormalities on ASD onset and progression at cellular and molecular levels.
- To explore potential therapeutic strategies targeting microglia for ASD.
Main Methods:
- Review of recent scientific literature on microglia and ASD.
- Analysis of studies detailing microglial morphology, function, and genetic/epigenetic factors in ASD models.
- Examination of molecular mechanisms, including neuroinflammation and synaptic alterations.
Main Results:
- Microglia in ASD models exhibit diverse abnormalities in morphology, function, and genetic expression.
- These dysfunctions contribute to neuroinflammation and aberrant synaptic pruning, impacting neural development.
- Specific molecular pathways affected include cytokine signaling and transcription factor activity.
Conclusions:
- Microglial dysfunction is a key factor in ASD pathogenesis.
- Targeting microglial pathways may offer novel therapeutic and preventative strategies for ASD.
- Further research into microglial roles is crucial for understanding and treating ASD.
