The University of Texas Southwestern in Dallas has recognized two possible new treatments for autism spectrum disorder, targeting the impact of a faulty gene on neural communication. Autism it a serious developmental disorder that weakens the ability to communicate and interact. It often works as a canopy for autism spectrum disorder (ASD). It is categorized by repetitive behaviors, and impaired social communication. According to the Centers for Disease Control and Prevention (CDC), around 1 in 68 children in the United States have been diagnosed with ASD. Treatments for ASD often focused on addressing the behavioral symptoms and helping people with the disorder to learn better communication strategies. Till now, very few efforts have targeted the biological causes of autism.
The two potential treatments that could restore the neurotransmission processes affected by the absence of a gene known as KCTD13. JCTD13 gene encodes a protein with the same name, and its expression level have linked with abnormal brain size, arguing on the loss and the gain of the chromosomal segment that contains this gene consult a substantial risk of autism and evolving delay. KCTD13 is not tied to the size of the brain but it is tied to synaptic transmission, or neurotransmission; this is the neurons ability to transmit information. KCTD13 deletion did not result in increased brain size, increased embryonic cell proliferation, and changes in migration. The deletion of KCTD13 impairs brain function in a major way, and they found a way to repair the damage, but they have more work to do before they try these treatments on people. The findings give us a clue as to what pathways are altered and where to look. The absence of KCTD13, increases the level of RhoA (a protein) which impairs synaptic transmission. To counteract the effect of the gene deletion, the researchers of the University tested different types of RhoA-inhibition drugs: Rhosin and Exoenzyme C3.
Rhosin and Exoenzyme C3 were successful in restoring normal synaptic transmission in under 4 hours, the incubation of brain slices in RhoA inhibitors could reverse synaptic abnormalities within the relatively short time frame of a few hours. Exoenzyme C3 is currently being tested in clinical trails for the treatment of spinal cord injury. If successful, they hope that these trials will smoothen the path for further tests of the drug’s potential in ASD treatments, as well. First, we would like to know if RhoA levels are altered in the mouse, who lacks the chromosomal segment that contains KCTD13. Secondly, determine if the abnormal locomotor behavior in the KCTD13 mice might be rescued by treatment of the whole animal with RhoA inhibitors. And in the end, genetic models of autism were predicted to alter the RhoA pathway.
Cohut, M. (2017, November 02). Experimental drugs rewire brain connections in autism.
Retrieved November 08, 2017, from https://www.medicalnewstoday.com/articles/319945.php
Washington University School of Medicine. (2017, November 2). In autism, too many brain connections may be at root of condition: Learning, social issues may reflect neuronal miscommunication. ScienceDaily. Retrieved November 10, 2017 from www.sciencedaily.com/releases/2017/11/171102131330.htm
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