Changes in diagnostic practices, more active neighborhood networks, and an increase in the number of older parents may all contribute to the massive rates of autism in California, says a group of social scientists. But the numbers still don’t add up.
Mouse models of fragile X syndrome show defects in two kinds of potassium channels — ubiquitous pores that control the flow of electrical current across neurons — in a brain area that processes sound, according to two papers published this summer.
The Autism Birth Cohort, based on data from 100,000 Norwegian children and their families, aims to uncover genetic and environmental factors contributing to the disorder.
An imaging study widely interpreted as heralding a diagnostic brain scan for autism is more preliminary than popular media reports would indicate, according to experts familiar with the work.
Researchers have uncovered an important molecular piece of a learning mechanism that occurs at the junction between neurons. The findings, which may help understand how the brain is disrupted in disorders such as autism, appear in the 24 June issue of Neuron.
Not all stem cells are created equal, a string of new studies suggests: adult cells that are reprogrammed into stem cells carry chemical remnants of the tissue from which they originate, making them distinct from embryonic stem cells. These differences may have important implications for studying fragile X syndrome and other diseases that arise from epigenetic glitches.
Racial minorities are under-represented in genetic studies, in part because research guidelines do not account for differences in family structure, according to a report based on statistics from several autism gene banks. In response to the report, research teams at Stanford University and the University of California, Los Angeles, are revamping their recruitment practices.
Toddlers who abruptly lose language, social or other developmental skills are more likely to have severe autism a few years later compared with children who have consistent delays from an early age. That’s the conclusion of the largest study thus far of autism onset patterns, published in the Journal of Autism and Developmental Disorders.
Scientists have for the first time captured a dynamic picture of brain defects in young mouse models of fragile X syndrome. The findings appeared in June in the Journal of Neuroscience.
Scientists have discovered that neurexins — proteins linked to autism — bind to a wide variety of molecules at the junction between neurons. In this complicated system, the breakdown of any one of the parts could lead to improper cell signaling, ultimately giving rise to disease.