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.
References:
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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