Molecular mechanisms: Lithium treats fragile X in mice
Lithium alleviates the symptoms of fragile X syndrome in mice in part by normalizing protein synthesis in the brain, according to a study published 29 December in Neurobiology of Disease.
Lithium alleviates the symptoms of fragile X syndrome in mice in part by normalizing protein synthesis in the brain, according to a study published 29 December in Neurobiology of Disease.
Some forms of autism are caused by too many proteins at the synapse, the junction between neurons, whereas other forms result from too few, according to a study published 23 November in Nature.
Neurons from mice that model fragile X syndrome may fire signals more readily than neurons from controls, according to a study published 5 October in The Journal of Neuroscience. The results suggest a cause for the high incidence of seizures in individuals with the syndrome.
A protein involved in the cascade of interactions at the junctions between neurons points to a potential therapy for fragile X syndrome, according to unpublished data presented at the 2011 Society for Neuroscience annual meeting in Washington, D.C.
The fragile X protein FMRP helps make proteins at the synapse, the junction between neurons, even when the genetic instructions for doing so are located far away in the nucleus, says Kimberly Huber.
Postmortem brains from adults with autism have lower-than-normal levels of the fragile X mental retardation protein, which is missing in individuals with fragile X syndrome.
A new review suggests that sleep problems in neurodevelopmental disorders don’t just reflect underlying weaknesses in neural circuitry; they actively intensify these deficits.
A compound that shows promise as a treatment for fragile X syndrome alleviates repetitive behaviors in mice, but unexpectedly makes them less social.
The protein missing in people with fragile X syndrome regulates the activity of more than 800 other proteins, including some key players in autism, according to a study published 22 July in Cell. Many of these autism-associated proteins cluster on either side of the synapse, the junction between neurons.
Small fragments of RNA, called microRNAs, can fine-tune the levels of proteins at the junctions between neurons in response to cell signals, according to a study published 10 June in Molecular Cell.