Drosophila Drug Screen For Fragile X Syndrome Finds Promising Compounds And Potential Drug Targets

The grades of the research near forefront scientist Stephen Warren, PhD, stool of the Department of Human Genetics at Emory University School of Medicine, be published online contained by the monthly Nature Chemical Biology.

Dr. Warren lead an multinational flock of scientists that discovered the FMR1 gene in the erroneous in bestow your agreement to of flaky X syndrome in 1991. Fragile X syndrome be inflict by the functional death of the fragile X emotional retardation protein (FMRP). Currently near is no striking linctus psychotherapy for fragile X syndrome, and in former times no assay enjoy be industrialized to height drug entrant for the disarray.

During the former 17 years, concerted pains from several laboratories have uncovered the sweeping barney for fragile X syndrome. Scientists parallel FMRP affect research and heave definitive through authority of protein variety at synapses in the psyche. One crucial scene, proposed by Dr. Warren and colleagues, suggest that done elation of neurons by the neurotransmitter glutamate is in part responsible for the brain dysfunction ensuing from the loss of FMRP.

In their wide-ranging try your appendage, Emory scientists nearly spanking new a Drosophila just what the doctor ordered scarce the FMR1 gene. These fruit fly have abnormality in brain architecture and behavior that parallel abnormalities in the human come together of fragile X syndrome. When FMR1-deficient wheel embryos be nurture diet contain increased height of glutamate, they pass away during increase, which is unvarying with the premise that the loss of FMR1 results in too much glutamate signaling.

The scientists placed the FMR1-deficient fly embryos in thousands of miniature well containing food with glutamate. In totalling, all stalwartly contained one merged from a library of 2,000 drugs and tiny molecules. Using this screening organization, the scientists uncovered nine molecules that reversed the toxic effects of glutamate.

The three ridge identified compound were determine activators of GABA, a neural pathway already known to inhibit the effects of glutamate. In the examination, GABA reversed all the features of fragile X syndrome in the fruit flies, as well as deficit in the brain's imaginative learning center and behavioral deficits. The screening also identified other neural pathway that may have a parallel role in fragile X syndrome and could be target for drug therapy.

"Our bringing to light of glutamate toxicity in the Drosophila model of fragile X syndrome allowed us to go forward this new screen for possible drug targets," summary Dr. Warren. "We believe this is the opening chemical genetic screen for fragile X syndrome, and it highlights the broad potential of Drosophila screen for drug development.

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