A drug previously intended for the treatment of obesity has been found to block cerebral receptors responsible for abnormal neuronal expressions. Researchers at the University of the Basque Country and the Achucarro neurosciences centre found that the pharmaceutical drug Rimonabant, which was taken off the market due to presumed psychiatric consequences, may be beneficial when utilized in a different context than once intended. Researcher Susana Mato remarks on the safety of the recalled drug saying, “[it] has been used a lot in preclinical research into the endocannabinoid system and it’s action mechanism is very well established.” The endocannabinoid system is the regulatory body of neuronal expressions characteristic of Fragile X Syndrome and Autism Spectrum Disorders (hypo- or hypersensitivity, attention deficit, anxiety, epileptic crisis, etc.) The researchers genetically modified mice to lack the FMRP protein, deficiency of which defines Fragile X Syndrome, and introduced Rimonabant. The experiment found that the drug blocks CB1 cannabinoid receptors thus normalizing sensory sensitivity and epileptic crises. While this is not a cure for Fragile X, which is a genetic disorder, the research findings near a reversal of symptoms—a significant stride in developmental disability research. To apply these findings, further research must first be done to test the appropriate dosages for humans and then clinical trials must be enacted. Having already passed preclinical stages, due to its former use for obesity treatment, the drug is on the fast track for Fragile X therapy. The full research findings are published in Nature Medicine. To read more about the experiment, visit: http://www.medicalnewstoday.com/releases/258952.php.
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