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.
Alterations in inhibitory circuits and difficulties in social recognition characterize mice missing one copy of DYRK1A, a gene linked to autism.
Increasing or reducing the levels of the UBE3A gene, which is associated with autism and autism-related syndromes, results in altered patterns of synaptic pruning — a process that snips away brain cell connections.
Synaptic changes in the brain region could drive a core trait of fragile X syndrome, a new mouse study suggests.
A protective pathway that pauses protein synthesis is muted in a mouse model of fragile X syndrome, according to a new study.
The map, by far the largest one of an entire brain to date, contains 130,000 neurons and 53 million synapses.
But multiple independent researchers say they are not convinced by its results, which fail to confirm high-profile findings from 2017.
Mice with microglia missing receptors for the neurotransmitter serotonin since birth have too many synapses and show social difficulties in adulthood.
Many genes related to the condition play a role in the internal scaffolding of cells, and cytoskeletal disruptions can affect neurodevelopment and behavior.
The approach improves the function of SYNGAP1-deficient neurons in vitro, but whether it will work in people remains unclear.