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Autism Spectrum Disorders (ASD) consist of a set of complex neurodevelopmental disorders characterised by impaired communication and social behaviour, and repetitive or stereotyped pattern of behaviour. The prevalence of ASD has increased in recent decades to 0.6-1% [1-3]. Broadening of the diagnostic criteria and increased awareness of autism among parents and health professionals likely contribute to the prevalence increase. However, the reason for the increase is not completely understood. Alterations of developmental processes and gene expression profiles have been identified in ASD but neuronal mechanisms and perturbations of neuronal networks underlying the ASD phenotype are unclear. ASD varies in severity and the clinical phenotype reflects multifactorial background [4]. Co-morbidity with some genetic syndromes and autism exist [5]. Affected males outnumber females roughly 4:1 [6-8]. The family studies imply that the autism has a strong genetic basis but no single high risk genes for ASD are identified [9]. Hundreds of de novo mutations with extreme locus heterogeneity have been identified in genes encoding protein network ranked for autism candidate genes [10]. Recent studies suggest that environmental factors could play a much larger role in susceptibility to ASD than earlier expected [4]. Since the population’s genetic inheritance is relatively constant over longer periods, the increased incidence rate of autism during last decades could indicate that there is an important environmental component in the etiology of autism [11].

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Oxidative Stress and Dietary Interventions in Autism: Exploring the Role of Zinc, Antioxidant Enzymes and Other Micronutrients in the Neurobiology of Autism