Co-PI's: Anne F. Simon M.S., Ph.D., Assistant Researcher Geneticist; and David E. Krantz, MD, Ph.D. Assistant Professor
Brain Research Institute, Department of Psychiatry and Biobehavioral Sciences, UCLA
Abstract and Specific Aims
Autistic patients show a profound impairment in the perception and response to social cues. Like most other aspects of autism, the mechanism underlying this phenotype is not known. Furthermore, the neural pathways that mediate social interactions in humans and animals remain poorly understood. The model organism Drosophila melanogaster has been used previously to study the genetic components of social behaviors such as courtship and aggression. Although the neuroanatomy of Drosophila differs significantly from that of mammals, they employ remarkably conserved mechanisms of synaptic transmission and cellular signaling. In addition, complex behavior in both flies and mammals is modulated by dopaminergic and serotonergic projections in the CNS. We propose to use Drosophila to study the genetics of social behavior, and the ability of Drosophila to perceive and respond to the presence of other flies. Preliminary data suggest that relatively straightforward assays we have developed can be used to quantitate this response, and that robust behaviors such as locomotion and grooming can be influenced by social contact between flies. We will now develop these assays further, including the generation of computer assisted methods to automate measurements of social interactions. These refinements will allow us to quantitate social interactions in large numbers of mutant lines. To investigate the genetic control of social behavior we will analyze the effects of candidate, modulatory pathways on fly social behavior. We have found that aminergic signaling pathways have potent effects on the behavior of individual flies. We have also found that mutations in the genes white and garnet, known to affect eye pigmentation and courtship, may have additional effects on social behavior. These data will provide a basis for a screen to genetically identify the genes required for the social response to the presence of another, similar animal, and to map the neuronal circuitry responsible for social behavior in flies. Since many of the pathways for normal neural function and disease processes are conserved between Drosophila and humans, we hypothesize that these data may be relevant to the genetic basis of social deficits in autism.
PI: Jeffrey J. Wood, Ph.D., Assistant Professor
UCLA Department of Education
Abstract and Specific Aims
Children and adolescents with high-functioning autism (HFA) and Asperger syndrome are at heightened risk for anxiety disorders
when compared with neurotypical children. The high prevalence rate of anxiety disorders in HFA is suggestive of a distinct subgroup
of children on the autism spectrum—an “anxious-inhibited” subgroup. Due to complications that a diagnosis of an anxiety disorder
can add to the adaptive functioning of children with HFA or Asperger syndrome that is above and beyond the difficulty
caused by the autism spectrum disorder—such as severe difficulty with adaptive functioning in academic, family,
and social settings—addressing anxiety disorders found in children with HFA is necessary. This study is designed to examine
the efficacy of a modified cognitive behavioral therapy (CBT) program designed specifically to remedy anxiety symptoms experienced
by children with HFA or Asperger syndrome who also have a clinically significant anxiety disorder.
Please contact Amy Drahota by phone at (310) 882-0537 or by email at adrahota@ucla.edu
for more information about this research.
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