Signaling imbalance in mutant mice supports key autism theory
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.
Rare or common, inherited or spontaneous, mutations form the core of autism risk.
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.
A new method uses mutations in DNA to maintain a detailed record of series of cellular events.
New findings hint at why drugs that work in mouse models of fragile X syndrome have not been effective in people.
A molecule made by mitochondria, the energy factories of cells, might help doctors forecast the impact of mutations in a top autism gene.
The largest analysis of sequences from autistic people and their families implicates 184 genes in the condition — nearly doubling the previous estimate.
Molecular biologist Jonathan Mill is probing gene expression’s role in autism in uncharted territory — the fetal human brain.
SETD5, a leading candidate for autism risk, may control thousands of genes by modifying a protein involved in packaging DNA.
Deleting the mutation from an autism gene may reverse some autism traits in mice, according to a new study. But the results may be a fluke.
An analysis of genetic sequences from nearly 500 people with autism and their relatives has linked 13 new genes to the condition. It has also uncovered a genetic cause for autism in about 10 percent of the autistic participants.
New findings call into question a fundamental assumption about how genes are regulated.