Contributors: Universität Heidelberg Heidelberg = Heidelberg University; Goethe-Universität Frankfurt am Main; King‘s College London; Universität Wien = University of Vienna; IFR49 - Neurospin - CEA; Commissariat à l'énergie atomique et aux énergies alternatives (CEA); Universiteit Utrecht / Utrecht University Utrecht; University of Cambridge UK (CAM); Radboud University Nijmegen; Radboud University Medical Center Nijmegen; Karolinska Institutet Stockholm; Stockholm Health Care Services (SLSO); The University of Western Australia (UWA); Génétique humaine et fonctions cognitives - Human Genetics and Cognitive Functions (GHFC (UMR_3571 / U-Pasteur_1)); Institut Pasteur Paris (IP)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité); Universität Zürich Zürich = University of Zurich (UZH); University of London London; University of Toronto; National Taiwan University Taiwan (NTU); Istituto Italiano di Tecnologia (IIT); Università degli Studi di Modena e Reggio Emilia = University of Modena and Reggio Emilia (UNIMORE); Centro de Investigación Biomédica en Red Salud Mental Madrid (CIBER-SAM); Karakter Child and Adolescent Psychiatry University Centre Nijmegen; This work was supported by EU-AIMS (European Autism Interventions), which received support from the Innovative Medicines Initiative Joint Undertaking under grant agreement no. 115300, the resources of which are composed of financial contributions from the European Union’ s Seventh Framework Programme (grant FP7/2007-2013), from the European Federation of Pharmaceutical Industries and Associations companies’ in-kind contributions, and from Autism Speaks. The results leading to this publication have received funding from the Innovative Medicines Initiative 2 Joint Undertaking under grant agreement No 777394 for the project AIMS-2-TRIALS. This Joint Undertaking receives support from the European Union's Horizon 2020 research and innovation programme and EFPIA and AUTISM SPEAKS, Autistica, SFARI.; European Project: 115300,EC:FP7:SP1-JTI,IMI-JU-03-2010,EU-AIMS(2012); European Project: 777394,H2020-JTI-IMI2-2016-10-two-stage,AIMS-2-TRIALS(2018)
نبذة مختصرة : International audience ; BackgroundReward processing has been proposed to underpin the atypical social feature of autism spectrum disorder (ASD). However, previous neuroimaging studies have yielded inconsistent results regarding the specificity of atypicalities for social reward processing in ASD.AimsUtilising a large sample, we aimed to assess reward processing in response to reward type (social, monetary) and reward phase (anticipation, delivery) in ASD.MethodFunctional magnetic resonance imaging during social and monetary reward anticipation and delivery was performed in 212 individuals with ASD (7.6–30.6 years of age) and 181 typically developing participants (7.6–30.8 years of age).ResultsAcross social and monetary reward anticipation, whole-brain analyses showed hypoactivation of the right ventral striatum in participants with ASD compared with typically developing participants. Further, region of interest analysis across both reward types yielded ASD-related hypoactivation in both the left and right ventral striatum. Across delivery of social and monetary reward, hyperactivation of the ventral striatum in individuals with ASD did not survive correction for multiple comparisons. Dimensional analyses of autism and attention-deficit hyperactivity disorder (ADHD) scores were not significant. In categorical analyses, post hoc comparisons showed that ASD effects were most pronounced in participants with ASD without co-occurring ADHD.ConclusionsOur results do not support current theories linking atypical social interaction in ASD to specific alterations in social reward processing. Instead, they point towards a generalised hypoactivity of ventral striatum in ASD during anticipation of both social and monetary rewards. We suggest this indicates attenuated reward seeking in ASD independent of social content and that elevated ADHD symptoms may attenuate altered reward seeking in ASD.
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