SEOUL, Oct. 28 (Korea Bizwire) — A new study has proven for the first time that the gene that causes Down’s syndrome could also bring about autism.
A joint research team consisting of members from the Korea Biotechnology Research Association and Augusta University in the U.S. revealed through an animal model using zebrafish on October 27 that DYRK1A, the Down’s syndrome-causing gene, could also work to produce autism.
Autism, which is also referred to as Autistic Spectrum Disorder (ASD), is an intellectual disability associated with having difficulties with social communication.
According to the result of a complete enumeration epidemiological survey in 2011, the autism prevalence rate among South Korean children between the ages of 7 to 12 was 2.64 percent, more than double the figure for children in the same age group (1 percent) in the US.
Though the reasons why the disease occurs is yet unclear, it is generally understood that autism is attributed to a combination of genetic and environmental factors working together.
In order to uncover the genetics leading to autism, the research team first made a zebrafish knockout mutant without the DYRK1A genetic function by using CRISPR, the genetic editing technology which enables cutting and attaching DNA.
As zebrafish have genetic structures very similar to humans, they are often used as animal models.
The research team developed the new validation method to measure sociality, which is the core aspect of ASD, on the grounds that zebrafish show strong intimacy to each other and swim in schools.
As a research outcome, zebrafish devoid of the DYRK1A genetic function were indifferent to other individuals and displayed a lack of sociality, which is a typical characteristic of ASD.
“We were able to verify the correlation between autism and DYRK1A, the high-risk gene most frequently found in ASD patients through an animal model for the first time in the world.” said chief researchers Kim Cheol-hee and Dr. Lee Jeong-soo. “The findings will contribute to the development of ASD medicines controlling the vitality of DYRK1A.”
Lina Jang (email@example.com)