Researchers have identified a potential molecular mechanism that causes Fragile X syndrome in the developing fetal brain.
Fragile X syndrome patients with prematuration had a much earlier onset of neurological problems, including earlier symptoms of neurodegeneration. They also experienced emotional processing problems. Some of the most common emotional processing disorders reported were mood regulation, anxiety, and psychosis.
Study reports repeats in genes associated with Fragile X syndrome normally regulate how and when proteins are made in neurons.
Sleep disruptions are common features of Fragile X syndrome, Williams syndrome, and Down syndrome. The disruption of sleep in these neurodevelopmental disorders appears to be linked to language development. The longer children with neurodevelopmental disorders slept, the more words they knew.
Stem cell study reveals a genetic defect associated with fragile X syndrome delays the production of neurons during a critical stage of embryonic development.
Lovastatin, a common statin usually prescribed to control cholesterol, corrected learning and memory deficits associated with Fragile X syndrome in rodent models.
Researchers report functional alterations in L-type calcium channels were detected in models of Fragile X syndrome.
Researchers have successfully reduced some symptoms associated with fragile X syndrome in mice with the help of CRISPR-Cas 9 gene editing.
According to researchers, a drug approved by the FDA may reverse some of the symptoms associated with Fragile X syndrome. The drug can reverse hyper-excitability that leads to sensory hypersensitivity.
Researchers shed new light on neuroplasticity by sparking learning in tadpole brains. They discovered the key to neuroplasticity is how the brain generates new proteins. Findings could help deepen understanding of sensory processing in ASD.
A new neuroimaging study reveals babies with Fragile X syndrome have less developed white matter in the brain compared to children without the condition.
Researchers report neurons in mice with a genetic defect that causes Fragile X are similar to those in mice without the syndrome, but fail to interact correctly. This failure results in the cognitive impairment associated with FXS.
