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Published on: October 17, 2025
Microglia in the pathogenesis of autism spectrum disorders
1Laboratory of Chemical Pharmacology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Japan.
Abstract:
Proper synaptic pruning is essential for the development of functional neural circuits. Impairments in synaptic pruning disrupt the excitatory versus inhibitory balance (E/I balance) of synapses, which may cause neurodevelopmental disorders such as autism spectrum disorder (ASD). Recent studies have determined molecular mechanisms by which microglia, the brain's resident immune cells, engulf inappropriate and less active synapses. Thus, microglial dysfunction may be involved in the pathogenesis of ASD through attenuated or excess synaptic pruning. In this review, we discuss recent animal and human studies that report an E/I imbalance and the characteristics of microglia in ASD. We will further discuss whether and how synaptic pruning by microglia is involved in the pathogenesis of ASD.
Insights
Microglia, the brain immune cells, play a key role in synaptic pruning essential for neural development. Their dysfunction may contribute to neurodevelopmental disorders like autism spectrum disorder (ASD) by altering synaptic balance.
Area of Science:
- Neuroscience
- Immunology
- Developmental Biology
Background:
- Proper synaptic pruning is crucial for developing functional neural circuits.
- Disruptions in synaptic pruning can lead to an imbalance in excitatory and inhibitory synapses (E/I balance).
- This E/I imbalance is implicated in neurodevelopmental disorders, including autism spectrum disorder (ASD).
Purpose of the Study:
- To review the role of microglia in synaptic pruning and its connection to ASD.
- To discuss findings on E/I imbalance and microglial characteristics in ASD.
- To explore the involvement of microglial synaptic pruning in ASD pathogenesis.
Main Methods:
- Review of recent animal and human studies.
- Analysis of research on E/I balance in ASD.
- Examination of microglial characteristics and function in ASD models.
Main Results:
- Microglia are identified as key players in engulfing synapses during pruning.
- Microglial dysfunction, leading to abnormal pruning (either too little or too much), is linked to ASD.
- Studies report altered E/I balance and specific microglial features in individuals with ASD.
Conclusions:
- Microglial dysfunction in synaptic pruning is a potential mechanism contributing to ASD pathogenesis.
- Understanding microglial roles in synaptic pruning may offer new therapeutic targets for ASD.
- Further research is needed to elucidate the precise mechanisms linking microglial activity to ASD outcomes.
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