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.
Two compounds that enhance the activity of BDNF, a protein needed for the growth of neurons, improve motor skills in mouse models of Rett syndrome and increase the mice’s lifespan.
A compound that boosts inhibitory signals in the brain could treat hyperactivity and excitability in mice that model fragile X syndrome, according to a study published 8 November in Developmental Neuroscience.
Despite funders’ requirements to share mouse models after publication, many researchers hoard the animals for the good of their labs — and that could have an adverse effect on the field as a whole.
SP1, a protein that regulates the expression of several autism candidate genes, could increase risk of the disorder by simultaneously altering the expression of a number of the genes, according to a study published 24 October in Biological Psychiatry.
Studying the cellular and molecular mechanisms that underlie autism is crucial to advancing our understanding of the disorder, says neuroscientist Eric Kandel.
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.
Three mutations in SHANK2, an autism-associated gene, each lead to abnormal synapses, the junctions between neurons, according to a study in Human Molecular Genetics.
There are a host of problems with laboratory rodents that scientists rarely talk about, argues a fascinating series of articles in Slate magazine.
Altered function of a brain receptor may help explain the why infection during pregnancy raises the risk for schizophrenia in the offspring, according to an unpublished rat study presented at the 2011 Society for Neuroscience annual meeting in Washington, D.C.