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Genetic Links To Impaired Social Behavior In Autism

Date:
May 14, 2008
Source:
Elsevier
Summary:
Individuals with autism spectrum disorders show profound deficits in social interactions and communications and display repetitive behaviors and abnormal responses to sensory experiences. One aspect of an autistic child's impaired social abilities is their lack of affiliative behaviors, i.e., behaviors such as touching and hugging that strengthen social bonds.
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Individuals with autism spectrum disorders (ASD) show profound deficits in social interactions and communications, and display repetitive behaviors and abnormal responses to sensory experiences. One aspect of an autistic child's impaired social abilities is their lack of affiliative behaviors, i.e., behaviors such as touching and hugging that strengthen social bonds. On May 15th, Biological Psychiatry is publishing an article that reports new findings on genetic bases of these behaviors.

In this study, Yale University researchers recruited, genotyped, and clinically assessed a large sample of autistic children and their families. They specifically examined the genetic variants in six genes known to be involved in maternal and affiliative behaviors. Dr. Elena Grigorenko, the senior author, discusses their study, "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 behaviors in ASD." The strongest statistical findings of the study implicate the prolactin gene, the prolactin receptor gene, and the oxytocin receptor gene in these affiliative behavior 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, comments, "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 adds, "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."


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Journal Reference:

  1. Genes Controlling Affiliative Behavior as Candidate Genes for Autism. Authors: Carolyn M. Yrigollen, Summer S. Han, Anna Kochetkova, Tammy Babitz, Joseph T. Chang, Fred R. Volkmar, James F. Leckman and Elena L. Grigorenko. Carolyn Yrigollen, Tammy Babitz, and Drs. Volkmar, Leckman and Grigorenko are affiliated with the Child Study Center at Yale University in New Haven, Connecticut. Drs. Volkmar, Leckman and Grigorenko are also with the Department of Psychology, while Summer Han, Anna Kochetkova and Dr. Chang are with the Department of Statistics, also at Yale University. Dr. Grigorenko is also with the Department of Epidemiology and Public Health at Yale University, and the Department of Psychology at Moscow State University in Russia. Biological Psychiatry, Volume 63, Issue 10 (May 15, 2008).

Cite This Page:

Elsevier. "Genetic Links To Impaired Social Behavior In Autism." ScienceDaily. ScienceDaily, 14 May 2008. <www.sciencedaily.com/releases/2008/05/080513101659.htm>.
Elsevier. (2008, May 14). Genetic Links To Impaired Social Behavior In Autism. ScienceDaily. Retrieved October 4, 2024 from www.sciencedaily.com/releases/2008/05/080513101659.htm
Elsevier. "Genetic Links To Impaired Social Behavior In Autism." ScienceDaily. www.sciencedaily.com/releases/2008/05/080513101659.htm (accessed October 4, 2024).

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