A new study by Yale University researchers has found that genetic factors play a major role in causing impaired social behaviour in individuals with autism spectrum disorders (ASD).
Washington, May 14 : A new study by Yale University researchers has found that genetic factors play a major role in causing impaired social behaviour in individuals with autism spectrum disorders (ASD).
People with ASD display profound deficits in social interactions and communications, and display repetitive behaviours and abnormal responses to sensory experiences. One aspect of an autistic child's impaired social abilities is their lack of affiliative behaviours, i.e., behaviours such as touching and hugging that strengthen social bonds.
After recruiting, genotyping, and clinically assessing a large sample of autistic children and their families, the scientists have now found the genetic bases of these behaviours. They specifically examined the genetic variants in six genes known to be involved in maternal and affiliative behaviours.
"Animal studies have taught us that genetic factors can play a crucial role in the development of close affiliative ties. With the help of Yale's Autism Center of Excellence, led by Drs. Ami Klin and Fred Volkmar, and many families of individuals with ASD, we have registered a possible association between some of the genes identified in animal studies as controlling affiliative behaviours in ASD," said Dr. Elena Grigorenko, the senior author of the study.
The study has mainly implicated the prolactin gene, the prolactin receptor gene, and the oxytocin receptor gene in these affiliative behaviour deficits.
John H. Krystal, M.D., Editor of Biological Psychiatry and affiliated with both Yale University School of Medicine and the VA Connecticut Healthcare System, said: "We are beginning to see that molecular genetics research is creating exciting new links between research in animal models and clinical disorders. The paper by Carolyn Yrigollen and colleagues suggests that two neurohormones that have been linked to affiliative behavior in animals, prolactin and oxytocin, are linked to deficits in affiliative behaviors associated with autism."
Dr. Grigorenko added: "This work builds on the most recent advances in genomics and the developmental neurosciences, and it sets the stage for a more extensive examination of our initial hypothesis. A clearer understanding of the genetic factors involved in ASD should result in new and better interventions for these devastating disorders."
The study will be published in Biological Psychiatry.
ANI