Mental health issues emerge with shifts in autism traits across childhood
Anxiety and other challenges autistic children experience may stem from an increase in social-communication issues and a decrease in repetitive behaviors from ages 6 to 11.
Anxiety and other challenges autistic children experience may stem from an increase in social-communication issues and a decrease in repetitive behaviors from ages 6 to 11.
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.
Both human and mouse progenitor cells with the alterations struggle to become neurons and instead express genes that are typically active only in muscle or the heart.
Dysfunctional circuits and a rogue sodium channel in the brainstem may explain the disordered breathing pattern seen in children with Pitt-Hopkins syndrome, a form of autism.
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.
Worms and zebrafish missing both copies of the gene CHD7 have disrupted cellular signaling, a dearth of inhibitory neurons and behavior changes — all of which are reversed by the stimulant drug ephedrine.
A new viral tool can selectively control different types of neurons that dampen brain activity in rodents, monkeys and people.
Autistic people who are hyperactive or have difficulty controlling their own impulses are the most likely to show ongoing self-injury.
The severity of autism tracks closely with that of attention deficit hyperactivity disorder.