Schizophrenia may be a consequence of neuronal birth gone awry, according to unpublished research presented today at the Society for Neuroscience conference.

Research on mouse models published in the past year is paving the way to reversing the symptoms of some autism-related disorders, National Institute Health directors told a packed room of 80 reporters at the morning at the Society for Neuroscience conference.

Brain tissue from individuals with autism is rare, to say the least: of the 30,000 samples in the National Institutes of Healthʼs Brain and Tissue Bank for Developmental Disorders, for instance, only 30 are from individuals diagnosed with autism.

A mouse model of neurofibromatosis ― a genetic neurodevelopmental disorder that leads to nerve tumors, memory problems and, often, autism ― exhibits deficits in social interaction and social learning, according to research presented in a poster session today at the Society for Neuroscience conference.

For decades, those who study brain cell activity have faced a fundamental trade off: either closely monitor the activity of a single cell or look at the circuit level to see how large groups of neurons communicate with each other.

Even as I type this, thousands of neuroscientists are descending on Washington D.C. for an annual event that is almost beyond description. An estimated 36,000 people are expected to attend Neuroscience 2008, this yearʼs meeting of the Society for Neuroscience, hobnob, listen to lectures, present posters and down drinks at the many social events.

Some small fragments of RNA are expressed differently in people with autism than in controls, according to two new studies. The findings unveil another layer of complexity in the genetics of autism.

Deletions or duplications of a specific segment of chromosome 16 ― which has previously been fingered as a ‘hotspotʼ for autism susceptibility ― may be present in a surprising number of people who don’t have autism, according to researchers presenting preliminary data today at the annual meeting of the Child Neurology Society in Santa Clara, California.

Mutations in the two genes that cause the disease tuberous sclerosis complex, or TSC, interfere with the normal formation of axons, the long and thin strands that conduct electrical signals between brain cells, researchers contend in a report in Genes and Development.

In imaging studies of children with autism, researchers are increasingly turning to methods that enhance natural sleep, rather than the traditional approach of sedating the children.