The Role of Oxidative Stress in Adults with Autism Spectrum Disorders

Friday, May 12, 2017: 5:00 PM-6:30 PM
Golden Gate Ballroom (Marriott Marquis Hotel)
M. B. Thorsen1, N. Bilenberg2, N. Heegaard3, Å. F. Svenningsen4 and T. M. Michel5, (1)Child and Adolescent Psychiatric dept, University of Souther Denmark, Odense, Denmark, (2)Child and Adolescent Psychiatry, Odense C, Denmark, (3)Department of Autoimmunology and Biomarkers, Statens Serum Institut, Copenhagen, Denmark, (4)Department of Neurobiology Research, Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark, (5)Psychiatric Dept, University of Southern Denmark, Odense, Denmark

The diagnosis of autism spectrum disorders (ASDs) is currently based on observational and anamnestic data. Despite many years of research into the underlying neurobiology, the etiology of autism is still not fully understood. Oxidative stress could be a key player in the pathogenesis.


As previous studies have focused on children, it is still not known whether oxidative stress is a temporal finding or a persistent key-player in the pathophysiology in ASD. We therefore aimed to investigate the levels of the classical antioxidants superoxide dismutase 1 and 2 in adults with ASD.


56 patients with a diagnosis of ASD, along with 56 age- and gender matched healthy controls, had their plasma analyzed for the antioxidants Copper/Zinc superoxide dismutase (SOD1) and Manganese superoxide dismutase (SOD 2) and filled out the autism quotient questionnaire (AQ).


Increased concentration of SOD1 was found among patients with ASD (268,2 vs. 205,6; p<0,0004), while no difference was found in SOD2 (85,06 vs. 76,21; p=0,5749). Patients with ASD scored higher on AQ (27 vs. 10; p<0,0001). When stratifying into AQ-score ≥ 32 vs. AQ-score < 32 no difference in SOD1 or SOD2 was found. There were baseline differences between case and control group, however none of them showed significant influence on either of the antioxidants.


Patients with ASD showed higher concentrations of the antioxidant superoxide dismutase 1. This could be the result of an upregulation of the protein synthesis due to increased exposure to oxidative stress. This could be a possible future therapeutic target, although more studies are needed.