Nutritional Neurobiology of Autism: Revisiting the Zinc Hypothesis
Recent data support a model in which altered zinc biology may act as a modifiable risk factor within a gene–environment interaction framework in autism. Disrupted zinc homeostasis may be a key mechanistic contributor to autism pathophysiology, and it is mimicked to some extent by other risk factors. This talk critically evaluates the hypothesis that ASD reflects a developmental zinc deficiency at the molecular and synaptic levels. The presentation will integrate molecular, genetic, nutritional, and translational evidence and address inconsistencies and methodological limitations in the field.
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