# Proof of Mechanism Study for the Treatment of Social Anhedonia in ASD

> **NIH NIH P50** · UNIVERSITY OF CALIFORNIA LOS ANGELES · 2020 · $286,244

## Abstract

PROJECT SUMMARY
Understanding the biological underpinnings of variation in social “wanting”, or lack thereof, in individuals with
ASD could open important areas for intervention. Despite solid evidence-based approaches for improving
social functioning in ASD, the majority of high-functioning adults with ASD remain isolated, with outcome
studies consistently noting little or no motivation to achieve relationships. Yet contrary to Kanner's original
hypothesis that autism is a ubiquitous “deficit in affective contact”, contemporary studies find extraordinary
variation in social behavior in ASD, with preservation of typical attachment behaviors, social cognition, and
social knowledge in many. Social neuroscience has revealed the importance of central nervous system
dopamine interactions with other systems such as neuropeptide signaling in normal social function, but
dopamine's role has not been carefully probed in people with ASD. This project proposes a proof of
mechanism study to test the hypothesis that individual differences in dopaminergic tone will help reveal
differences in social motivation, and that modification of dopaminergic tone will impact social “wanting” and
social reward responsivity. We plan to enroll a sample of high-functioning adolescents and young adults with
ASD who will be receiving a 16-week social skills training program. We will examine differences in indices at
multiple levels of social motivation and social reward, from: 1) neural reward circuit activation; 2) physiologic
responses; 3) affective responses to social interaction; and 4) social interest and enjoyment, at pre-treatment,
and during the placebo-controlled administration of a dopamine agonist. This project is synergistic with other
Center components, obtaining common measures of reward responsivity in Project 3, applying shared
Diagnostic and Phenotyping Core measures, and collecting biospecimens for combined genetic and other
analyses, enabling broader investigations of heterogeneity across age and gender. Project results will yield a
definitive “Yes” or “No” confirmation of dopamine as a possible treatment target for social dysfunction in ASD.
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## Key facts

- **NIH application ID:** 9984499
- **Project number:** 5P50HD055784-14
- **Recipient organization:** UNIVERSITY OF CALIFORNIA LOS ANGELES
- **Principal Investigator:** JAMES T. MCCRACKEN
- **Activity code:** P50 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $286,244
- **Award type:** 5
- **Project period:** 2007-08-06 → 2022-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9984499

## Citation

> US National Institutes of Health, RePORTER application 9984499, Proof of Mechanism Study for the Treatment of Social Anhedonia in ASD (5P50HD055784-14). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/9984499. Licensed CC0.

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