Protein probe may diagnose fragile X syndrome
Quick tests that detect the protein missing in fragile X syndrome can be used to screen newborns for the disorder and find treatments, according to two studies published in the past two months.
Quick tests that detect the protein missing in fragile X syndrome can be used to screen newborns for the disorder and find treatments, according to two studies published in the past two months.
The discovery of microRNAs that regulate gene expression has changed our view of cellular biochemistry. It may also change our perception of neuropsychiatric disorders such as autism, says Peng Jin.
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.
Researchers have uncovered a new role for the protein missing in fragile X syndrome — it regulates the release of neurotransmitters, chemical messengers in the brain, according to a mouse study published 20 February in Neuron.
A mild form of fragile X syndrome that can lead to the full syndrome in one generation is more common than previously thought, according to a large study published 21 December in Genome Medicine.
A number of autism risk factors converge on one cellular pathway: abnormal remodeling of the cell’s structural systems through the signaling protein Rho, says SFARI’s associate director for research, Alan Packer.
A growing number of studies suggest connections between Alzheimer’s disease, fragile X syndrome and autism, which could point the way to potential treatments.
The pupils of children with autism react to light more slowly and less efficiently than those of controls, according to a study published 18 December in the Journal of Autism and Developmental Disorders.
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.