Effects of a beta-adrenergic antagonist on social and cognitive abilities in autism spectrum disorder
Sunday, Nov 10, 2013, 1:00 PM - 2:00 PM
++C.07.c. Autism: Physiology and systems
*R. M. ZAMZOW
, B. J. FERGUSON, M. L. LEWIS, E. C. REZNICEK, A. S. RAGSDALE, S. E. CHRIST, J. P. STICHTER, D. Q. BEVERSDORF;
Univ. of Missouri-Columbia, Columbia, MO
Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by social communication impairments and restricted, repetitive behaviors. Current pharmacological interventions for ASD focus primarily on psychiatric symptoms, such as agitation and obsessive behaviors. Few agents target core domains, such as social and cognitive functioning. It has been previously hypothesized that stress contributes to social and cognitive deficits in ASD. Accordingly, propranolol, a non-selective beta-adrenergic antagonist with known anxiolytic effects, may serve as a potential therapeutic agent for ASD, as it blocks the noradrenergically mediated sympathetic response system. The present ongoing study explores the effects of propranolol on social and cognitive abilities in ASD. Individuals with ASD participated in two study sessions in which they were given propranolol (40 mg) or placebo in a counterbalanced, double-blinded manner. 60 minutes following drug administration, participants performed several cognitive and social tasks. Preliminary analyses indicate a significant improvement in task performance on the General Social Outcomes Measure, an assessment of social functioning, as well as a trend for improved task performance on the Anagrams task, a measure of problem solving abilities, in the propranolol condition, as compared to the placebo condition. Continued data collection is necessary to further characterize the effects of propranolol on social and cognitive abilities in ASD. In addition, subsequent work will consider the role of baseline sympathetic nervous system activity in predicting which individuals will respond best to propranolol. Overall, these findings contribute to insight regarding potential therapeutic interventions for core symptomatology in ASD.
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