Reactions from SfN 2013
Tune in for daily updates and reactions from attendees at the 2013 Society for Neuroscience meeting in San Diego, California.
Tune in for daily updates and reactions from attendees at the 2013 Society for Neuroscience meeting in San Diego, California.
A gene’s length may influence its expression, and this has implications for autism, which tends to be linked to particularly long genes, says Mark Zylka.
Researchers have uncovered the mechanism by which a candidate drug for Angelman syndrome activates UBE3A, the gene that is silenced in the syndrome, according to a study published 20 August in the Proceedings of the National Academy of Sciences.
Neurons derived from individuals who carry extra copies of an autism-linked chromosomal region have gene expression patterns that are unexpectedly similar to those of neurons with deletions of the region. The unpublished findings were presented Thursday at the Dup15q Alliance Scientific Meeting in Sacramento, California.
Long genes, and their relationship to a class of enzymes that regulate gene expression, raise intriguing questions about the risk for neuropsychiatric disorders.
Mice that express elevated levels of an autism-linked gene in the nucleus of neurons show social and communication problems, according to unpublished research presented Thursday at the Dup15q Alliance Scientific Meeting in Sacramento, California.
Enzymes called topoisomerases are crucial for the expression of extremely long genes, including many that have been linked to autism, according to a study published 5 September in Nature. The researchers also discovered that autism genes are, on average, significantly longer than others.
The autism-like features seen in related neurological disorders may be the result of intellectual disability and not a shared underlying biology, says Alan Packer.
Watch the complete replay of Benjamin Philpot discussing the possibility of pharmacologically turning on a silent gene to treat Angelman syndrome. Submit follow-up questions.
Depleting excess levels of a molecule involved in neuronal signaling prevents the cognitive and motor symptoms of Angelman syndrome in a mouse model of the disorder, according to a report published 15 August in Cell Reports.