Ongoing research from the University of Texas, Dallas has been successful in identifying potential treatments of ASD related disorders by accurately targeting the faulty genes arising out of neuronal communications.
The study has so far revealed information about interlinked autism genes that play different roles from what has been understood so far.
Autism, or Autism spectrum disorder, is a term that is used to describe characteristics arising out of monotonous behaviors and impaired social communication with limited focused interests.
As per the recent estimates available with the CDC, Center for Disease Control and Prevention, an average of 1 in every 68 children are seen to be diagnosed on the spectrum in the USA alone. Autism-related treatments are often seen to address issues arising out of behavioral symptoms in a bid to assist people with the condition in learning the techniques of picking up useful communication strategies.
In other words, efforts to understand the biological causes of the disorder often take a backseat.
In the current study, the team is exploring new routes of learning curves to understand the underlying biological factors affecting individuals diagnosed on the spectrum. The study is being led by Dr. Craig Powell, who along with the team has been successful in uncovering two potential treatments that are seen to assist in restoring neurotransmission processes.
The process is seen to be largely affected by the absence of an important gene, KCTD13.
Can the Missing Gene be responsible for impairing the function of the brain?
KSTD13 is a gene that encodes proteins with a similar name and multiple studies working to understand its behaviors have already stated the expression levels of the gene to be responsible in boosting the size of the brain to abnormal levels. The researchers argue that the gain and the loss of the chromosomal segments that are present in the gene contribute to risks for ASD disorders by a significant extent, leading to developmental delays.
However, the team led by Dr. Powell presents different results about the actual role of KCTD13. The gene is observed to be not completely tied up to the size of the brain, rather to synaptic and neurotransmissions of a human brain, where the neurons are capable of transmitting the received information.
Dr. Powell explains, “We deleted the KCTD13 gene and were quite taken aback by the obtained results. The deletion did not increase the size of the brain nor any changes related to migrations.”
This discovery led to the researchers identifying potential drugs that could help them reverse the faulty connectivity arising out of the gene’s deletion.
The researchers included genetically modified mice in their further studies and noted that the absence of the gene nearly presented half the total number of synapse connections in the animal brains.
The researchers further noted that in its normal expression, the gene works by allowing neurons to communicate freely.
In its normal expression, KTCD13 helps to regulate this protein, allowing neurons to communicate freely. The team further tested by having the normal synaptic transmissions restored in less than 4 hours.
The researchers finally expressed their ongoing interests to look at different genetic models to understand the alteration of RhoA pathways.