Najat O Hamed1,2, Laila Al-Ayadhi3,4,5, Mohamed A Osman1,6, Abdalla O Elkhawad7, Hanan Qasem4, Majida Al-Marshoud8, Nada M Merghani8, Afaf El-Ansary4,5,8. 1. Department of Medical Biochemistry, University of Medical Sciences and Technology, Khartoum, Sudan. 2. Department of Pharmacology, Almaarefa Colleges for Science & Technology (MCST), Riyadh, Saudi Arabia. 3. Department of Physiology, Faculty of Medicine, King Saud University, Riyadh, Saudi Arabia. 4. Autism Research and Treatment Center, King Khalid University Hospital, Riyadh, Saudi Arabia. 5. Shaik AL-Amodi Autism Research Chair, King Saud University, Riyadh, Saudi Arabia. 6. Department of Pharmacology, Faculty of Pharmacy, University of Medical Sciences and Technology, Sudan Medical and Scientific Research Institute, Khartoum, Sudan. 7. Kirkwood College, Iowa, USA. 8. Central Laboratory, Female Centre for Scientific and Medical Studies, King Saud University, Riyadh, Saudi Arabia.
Abstract
AIM: Autism is a heterogeneous neurological disorder that is characterized by impairments in communication and social interactions, repetitive behaviors, and sensory abnormalities. The etiology of autism remains unclear. Animal, genetic, and post-mortem studies suggest that an imbalance exists in the neuronal excitation and inhibition system in autism. The aim of this study was to determine whether alterations of the measured parameters in children with autism are significantly associated with the risk of a sensory dysfunction. METHODS: The glutamine synthetase (GS), kidney-type glutaminase (GLS1), and glutamic acid decarboxylase autoantibody levels were analyzed in 38 autistic children and 33 age- and sex-matched controls using enzyme-linked immunosorbent assays. RESULTS: The obtained data demonstrated significant alterations in glutamate and glutamine cycle enzymes, as represented by GS and GLS1, respectively. While the glutamic acid decarboxylase autoantibodies levels were remarkably increased, no significant difference was observed compared to the healthy control participants. CONCLUSION: The obtained data indicate that GS and GLS1 are promising indicators of a neuronal excitation and inhibition system imbalance and that combined measured parameters are good predictive biomarkers of autism.
AIM: Autism is a heterogeneous neurological disorder that is characterized by impairments in communication and social interactions, repetitive behaviors, and sensory abnormalities. The etiology of autism remains unclear. Animal, genetic, and post-mortem studies suggest that an imbalance exists in the neuronal excitation and inhibition system in autism. The aim of this study was to determine whether alterations of the measured parameters in children with autism are significantly associated with the risk of a sensory dysfunction. METHODS: The glutamine synthetase (GS), kidney-type glutaminase (GLS1), and glutamic acid decarboxylase autoantibody levels were analyzed in 38 autisticchildren and 33 age- and sex-matched controls using enzyme-linked immunosorbent assays. RESULTS: The obtained data demonstrated significant alterations in glutamate and glutamine cycle enzymes, as represented by GS and GLS1, respectively. While the glutamic acid decarboxylase autoantibodies levels were remarkably increased, no significant difference was observed compared to the healthy control participants. CONCLUSION: The obtained data indicate that GS and GLS1 are promising indicators of a neuronal excitation and inhibition system imbalance and that combined measured parameters are good predictive biomarkers of autism.