Microglial overreaction to atypical neurons may drive autism
In mice and organoids lacking a neuronal protein, microglia prune synapses to excess.
In mice and organoids lacking a neuronal protein, microglia prune synapses to excess.
The collection offers a glimpse into differences in cell composition — across people and brain regions — that may shape neural function.
Mice with microglia missing receptors for the neurotransmitter serotonin since birth have too many synapses and show social difficulties in adulthood.
The findings add to the growing evidence that genes with disparate functions can play similar roles in brain development.
The chimeric mouse model could provide a more realistic way to study microglia’s roles in brain conditions such as autism.
The changes may help explain the link between maternal infection and autism, though more research is needed.
Postmortem brain samples from people with one of six conditions, including autism, show distinct signatures of over- and underexpression of immune genes.
Having an infection during pregnancy is tied to a small increase in the chances of having an autistic child, but the connection may not be causal.
The approach could help test hypotheses about how atypical function of the brain’s immune cells contributes to autism.
The method yields complex organoids that more closely mimic embryonic brain development than do those cultured in other ways.