Some social issues in DYRK1A model mice stem from faulty inhibitory circuits
Alterations in inhibitory circuits and difficulties in social recognition characterize mice missing one copy of DYRK1A, a gene linked to autism.
Alterations in inhibitory circuits and difficulties in social recognition characterize mice missing one copy of DYRK1A, a gene linked to autism.
Early treatment with nutritional supplements and a high-protein diet forestalls some neurodevelopmental problems for children with BCKDK deficiency.
The gene helps neurons exit the cell-maturation cycle during fetal brain development, a new study shows. But male and female mice respond differently to DDX3X loss.
The first animal model of MYT1L syndrome suggests that fast-maturing neurons lead to the unusually small brains, social deficits and other traits seen in people with the condition.
A transplant of inhibitory neurons during the second week of life prevents social difficulties and a brain signaling imbalance in mice missing a copy of FOXG1.
A genetic therapy and an existing drug both restore typical brain size in mice missing DYRK1A, a top autism candidate gene, in the cerebral cortex, a new study shows. The animals typically have smaller brains than controls.
A screening technique tests how inactivated genes affect spheres of cultured brain cells; it could shed light on autism-linked mutations.
Some people with autism have an unusually large head. What causes the enlargement? And does it have any bearing on outcome?
Individuals with mutations in an autism gene called TRIO may have a range of conditions, including intellectual disability and anomalous head size.
A cellular pathway that helps neurons grow and move during fetal development may drive the changes in head size in some autistic people.