Conventional optogenetic manipulations to excite or inhibit neurons stop when the light switches off. A new approach makes the changes last.

Iama Therapeutics is hoping a new class of molecule will prove successful against an old target in autism.

Interneurons that fail to propagate electrical signals in mice that model Dravet syndrome may cause the animals, like people with the autism-linked condition, to die suddenly.

Altered electrical activity in the neurons of mice with a mutated copy of SCN2A may explain the animals’ autism-like social behaviors.

Deleterious mutations in an autism-associated gene can make neurons hyperexcitable, raising the risk of epileptic seizures.

Genetic sequences from nearly 53,000 people with autism, developmental delay or intellectual disability reveal strong ties to 98 genes.

Neurons derived from people with 22q11.2 deletion syndrome show deficits in calcium signaling and electrical activity, pointing to possible therapeutic targets.

A new, minimally invasive technique allows researchers to activate neurons in the brains of mice and monkeys by using a light source located outside of the head.

The mutation that causes Angelman syndrome makes neurons hyperexcitable, which may explain the frequent seizures that most people with the syndrome have.

Electronic neurons made from silicon mimic brain cells and could be used to treat conditions such as autism.