Three Decades of Valproate: A Current Model for Studying Autism
Spectrum Disorder

David      Zarate-Lopez; Ana   Laura   Torres-Chávez; Alma   Yadira   Gálvez-Contreras; Oscar      Gonzalez-Perez
doi:10.2174/1570159X22666231003121513
Abstract

Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder with increased prevalence and incidence in recent decades. Its etiology remains largely unclear, but it seems to involve a strong genetic component and environmental factors that, in turn, induce epigenetic changes during embryonic and postnatal brain development. In recent decades, clinical studies have shown that inutero exposure to valproic acid (VPA), a commonly prescribed antiepileptic drug, is an environmental factor associated with an increased risk of ASD. Subsequently, prenatal VPA exposure in rodents has been established as a reliable translational model to study the pathophysiology of ASD, which has helped demonstrate neurobiological changes in rodents, non-human primates, and brain organoids from human pluripotent stem cells. This evidence supports the notion that prenatal VPA exposure is a valid and current model to replicate an idiopathic ASD-like disorder in experimental animals. This review summarizes and describes the current features reported with this animal model of autism and the main neurobiological findings and correlates that help elucidate the pathophysiology of ASD. Finally, we discuss the general framework of the VPA model in comparison to other environmental and genetic ASD models.
Keywords: Autism spectrum disorder, valproic acid, HDAC inhibition, neurodevelopment, prenatal exposure, pathophysiology.
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DOI https://dx.doi.org/10.2174/1570159X22666231003121513	Print ISSN 1570-159X
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