Watch the complete replay of Kimberly Huber discussing the role of autism-linked genes in the natural pruning of brain cell connections. Submit your own follow-up questions.
Researchers can use light to activate certain proteins that receive signals at the junctions between neurons and that are key targets for fragile X syndrome therapies, according to a study published in the April issue of Nature Neuroscience.
Researchers have added two new candidates to the arsenal of compounds that alleviate both the behavioral and molecular hallmarks of fragile X syndrome in mice that model the disorder. A third candidate, minocycline, improves some symptoms in children with the disorder.
The protein lacking in fragile X syndrome works with three autism-linked proteins to fine-tune the connections between neurons, according to a study published 21 December in Cell.
FMRP, the protein missing in fragile X syndrome, binds to the RNA sequences of 939 genes, 93 of which have been linked to autism, according to a study published 20 December in Nature.
Postmortem brains from individuals with autism have astrocytes that are smaller but denser than in control brains, according to a study published 21 September in the Journal of Neuroinflammation. The researchers found similar alterations in a mouse that lacks the autism-linked gene NLGN3.
Four new studies of neuroligin-1 (NLGN1), a gene linked to autism, unravel its complex role in regulating the connections between neurons.