Bumetanide may benefit only a subset of autistic children
Contrary to previous results, the blood pressure drug did not uniformly improve autism traits in a new clinical trial.
Contrary to previous results, the blood pressure drug did not uniformly improve autism traits in a new clinical trial.
A growing number of studies are revealing circuits that may underlie social challenges in autism — and how to fine-tune them.
A new atlas lays bare how synapses, or the junctions between neurons, change from birth to old age in mice.
Nearly all genes with moderate to strong ties to autism are expressed in the developing amygdala; a few show altered expression in the amygdalae of autistic people.
Mice missing DLG2, a protein central to neuronal activity, are anxious, sleep poorly and overgroom themselves.
Mice missing an autism gene called SHANK3 tend to be hypersensitive to touch, which may stem from underactivity of neurons that normally dampen sensory responses.
Neurons in mice that lack an autism gene called CNTNAP2 do not differentiate well between social and nonsocial smells — an issue that seems to stem from haphazard neuronal firing.
Studies of Rett syndrome hint at genes, cells and brain circuits that may be involved in autism — and may pave the way to treatments for both conditions.
Mice missing a copy of CHD8, a top autism gene, show a signaling imbalance in their brains — a finding in line with a popular hypothesis about autism’s origins.
Families of children with mutations in a gene called SYNGAP1 have spurred research into the effects of the mutations on people — and how to treat them.