Abstract
Pre- and perinatal zinc deficiencies have been consistently linked to autism spectrum disorder (ASD) in epidemiological studies. Zinc plays a key role in neurodevelopment and is involved in the same processes that have been identified to be affected in humans and several ASD animal models that are based on the manipulation of genetic and other nongenetic factors. In mice, prenatal zinc deficiency results in ASD-like behavior. Besides, zinc supplementation ameliorated ASD symptoms in individuals with ASD. Therefore, the results of many studies provide a strong basis for a closer investigation of zinc as the prime trace metal involved in ASD, and these results will be summarized in this chapter. In particular, this chapter will go beyond correlation studies and present data that can link zinc deficiency mechanistically to the ASD pathology and other genetic and non-genetic risk factors for ASD.
Published Version
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