Abstract
Incidence of autism spectrum disorder (ASD) diagnosis is increasing worldwide. Multiple causes have been proposed to account for this rise, notably increased awareness, changes in diagnostic methods or better identification of underlying genetic mutations. Multiple data sets from epidemiological and experimental studies show that environmentally relevant chemicals, most often endocrine-disrupting chemicals (EDCs), can modify brain development, especially during fetal development. Many EDCs act through nuclear receptors that alter gene transcription through modulating epigenetic mechanisms. Thus, epigenetic modifications can exacerbate underlying gene mutations and hence contribute to the etiology of autism. Our research focuses on EDCs acting on thyroid hormone (TH) signaling, as TH is needed to orchestrate both prenatal and postnatal brain development. What is more, first, mothers lacking TH have an increased risk of giving birth to an autistic child, and second, it is known that many EDCs interfere with thyroid signaling at different levels.
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