An imbalance in the excitatory and inhibitory signaling between neurons seems to play a critical role in autism. What can we do with that information?
Loss of one copy of 22q11.2 — a chromosomal region linked to schizophrenia and autism — shifts the location of neurons that inhibit brain signals, according to a study published 6 November in Proceedings of the National Academy of Sciences.
In 2003, John Rubenstein and Michael Merzenich first described the theory, now popular in autism, that the disorder reflects an imbalance between excitation and inhibition in the brain. Takao K. Hensch and Parizad M. Bilimoria review the paper and its impact on the field.
Watch the complete replay of Vikaas Sohal’s webinar on abnormal neural circuits in autism. Submit your own follow-up questions.
Elevated levels of EIF4E, which plays a key role in protein synthesis, lead to autism-like behaviors and abnormal neuronal signaling in mice, according to a study published 17 January in Nature.
Bumetanide, a drug that’s long been used to treat high blood pressure, modestly improves social behaviors in children with mild forms of autism, according to the results of a small trial published in December in Translational Psychiatry.
Neurons in mice that model fragile X syndrome show immature, overexcitable firing patterns, particularly during sleep, according to unpublished research presented last week at the Salk Institute, Fondation IPSEN and Nature Symposium on Biological Complexity in La Jolla, California.
Memantine, a drug used to treat Alzheimer’s disease, can reverse autism-like features in mice lacking one copy of the MEF2C gene, according to a poster presented last week at the Salk Institute, Fondation IPSEN and Nature Symposium on Biological Complexity in La Jolla, California.
A new study bolsters the idea that overactive protein synthesis contributes to autism. The findings, published 21 November in Nature, show that dampening a single overabundant protein, neuroligin-1, reverses both abnormal brain activity and social deficits in mice.
The anxiety drug diazepam, commonly marketed as Valium, reverses deficits in sensory integration in a mouse model of autism, according to research presented Sunday at the Society for Neuroscience annual meeting in New Orleans.