A drug that helps promote gene expression reduces repetitive behaviors and improves memory and sociability in a mouse model of autism.
Rare or common, inherited or spontaneous, mutations form the core of autism risk.
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 new resource profiles gene expression and the accessibility of DNA in single cells across the developing human cerebral cortex and may help scientists decipher the effects of noncoding mutations linked to autism.
Spontaneous genetic mutations contribute to autism in 30 to 39 percent of all people with the condition, and 52 to 67 percent of autistic children whose siblings do not also have the condition.
Mock viral infections impair social memory in mice with a mutation tied to autism, and autistic boys are more likely than their non-autistic peers to have had serious infections early in life.
An advanced DNA-sequencing technique has identified gene-damaging mutations, some with ties to autism, in about 1 in 15 men.
The X chromosome holds stronger-than-expected genetic sway over the structure of several brain regions. The genes that may underlie this oversized influence have ties to autism.
A novel gene delivery system taps a protein found in people to encapsulate messenger RNA and transport it into cells.
Over the past century, scientists have used a variety of animal models to advance their understanding of the developing brain and autism.
In the past two decades, some autism researchers have turned to simple animals, such as roundworms, fruit flies and zebrafish, for their investigations. Others have sought answers from experiments with frogs, birds and even octopuses.