Microglial overreaction to atypical neurons may drive autism
In mice and organoids lacking a neuronal protein, microglia prune synapses to excess.
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In mice and organoids lacking a neuronal protein, microglia prune synapses to excess.
The chimeric mouse model could provide a more realistic way to study microglia’s roles in brain conditions such as autism.
The approach could help test hypotheses about how atypical function of the brain’s immune cells contributes to autism.
The in-depth approach shows mutations in the autism-linked gene disrupt neuronal growth and communication, as well as mitochondrial gene expression.