Fragile X syndrome--the most common heritable cause of autism spectrum disorder--is something of a phantom. It interferes with the production of a protein critical to synapse formation during a brief period in early development when the brain is optimizing its ability to process sensory input. Then it dials way down...leaving behind permanent changes in neural circuit structure that can cause low IQ, learning disabilities, and hypersensitivity, along with other symptoms characteristic of ASD. This picture of the basic nature of Fragile X has been reinforced by a series of studies reported in a paper titled "Fragile X Mental Retardation Protein Requirements in Activity Dependent Critical Period Neural Circuit Refinement" published in the August 7,2017 issue of Current Biology. The article is titled “Fragile X Mental Retardation Protein Requirements in Activity-Dependent Critical Period Neural Circuit Refinement.” The research was conducted by a team of researchers in the Broadie Laboratory at Vanderbilt University--Kendal Broadie, Stevenson Professor of Neurobiology, postdoctoral fellow Dr. Caleb Doll, and graduate student Dominic Vita--who employed a battery of state-of-the-art techniques to document the effects that the lack of a critical protein caused by the syndrome, called the Fragile X Mental Retardation Protein (FMRP), has on the development of the brain and nervous system of the Drosophila disease model."Our research confirms that the Fragile X protein is essential for refining the brain's ability to process sensory information. The brains of individuals with the syndrome look perfectly normal.
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