Creating neurons from stem cells in a lab dish is a popular approach for studying developmental disorders such as autism. But how closely these neurons resemble those found in an adult brain has been unclear. Two new methods, described 2 July in Neuron, suggest that these neurons recapitulate the early stages of development.
British psychologist Uta Frith has singlehandedly transformed our understanding of autism. In partnership with her husband, neuroimaging expert Chris Frith, she helped launch the field of cognitive neuroscience and shaped a generation of scientists.
To characterize people who carry deletions in 16p11.2 and 15q13.3, genetic regions linked to autism, two studies published this summer looked in detail at dozens of people with either deletion. The studies found that deletions in these regions lead to diverse symptoms that only sometimes include autism.
New estimates on the role of common mutations in autism raise questions about how to quantify and parse genetic risk. Three experts say both common and rare variants are worth pursuing.
The configuration of methyl groups that modify DNA in sperm change as men get older. These alterations may help explain why children of older fathers are at increased risk for neuropsychiatric disorders such as autism.
Autism pioneer Uta Frith reminisces about dramatic shifts in British researchers’ understanding of autism that effectively ended the institutionalization of children with the disorder.
Severe mental illness such as schizophrenia or bipolar disorder in a parent significantly ups autism risk.
A long-awaited report, published today in Nature, confirms that with access to tens of thousands of genomes, researchers can identify common genetic risk factors for a complex neuropsychiatric disorder.
Common genetic variants that have minor effects may contribute about half the risk of developing autism, according to a study published Sunday in Nature Genetics. Identifying these variants would require tens of thousands of samples.
A large international consortium is creating and characterizing thousands of mouse mutants, each of which lacks a single gene in the genome. The first 300 of these mutants are expected to be available later this month.