Abstract

Despite hundreds of different candidate genes and numerous nongenetic factors that have been linked to autism spectrum disorder (ASDs), ASDs are diagnosed by the presence of two characteristic behaviors that are present in individuals with ASDs, namely social impairments and repetitive and stereotypic behaviors. Therefore, all discussed causes for ASDs ultimately converge on these common behavioral abnormalities. Given that behaviors are the result of neurobiological processes, it is likely that the same processes are disturbed by all causative factors and that they show convergence not only on behavioral but also on the molecular level. Therefore, the question arises, what is the neurobiological mechanism that lies at the core of the ASD symptoms, and how can so many genetic and nongenetic factors be part of the same process? In this book, the influence of trace metals on the key molecular features that may play a role in ASD, such as oxidative stress, inflammation, synapse formation and synaptic signaling, brain connectivity, and gut–brain signaling, has been discussed. Thus, trace metal imbalances, through the plethora of processes that trace metals regulate, may be an interesting candidate for the core pathology of ASD, which would make ASD a group of metal deficiency diseases.

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