Skewed signaling in striatum may spawn repetitive behaviors
Synaptic changes in the brain region could drive a core trait of fragile X syndrome, a new mouse study suggests.
Synaptic changes in the brain region could drive a core trait of fragile X syndrome, a new mouse study suggests.
Knocking down the gene that codes for the proteins normalizes the vocalizations.
Many genes related to the condition play a role in the internal scaffolding of cells, and cytoskeletal disruptions can affect neurodevelopment and behavior.
The method yields complex organoids that more closely mimic embryonic brain development than do those cultured in other ways.
Mice missing the autism-linked SHANK2 and SHANK3 genes in their retrosplenial cortex have trouble distinguishing between novel and familiar mice.
Together, the neurons are part of the corticostriatal circuit, which has been implicated in autism.
A brain area called the tail of the striatum may account for the shift.
Mice missing a copy of the gene ASH1L have excess synapses and autism-like behavioral differences, some of which are reversed by boosting an ASH1L-regulated gene.
Atypical patterns of neuronal activity and gene expression in the striatum may characterize autism in girls, according to a new study.
Some neurons activate autism-linked genes when they fire, according to a new study.