Roles of Epigenetics and Glial Cells in Drug-Induced Autism Spectrum Disorder

TL;DR

This paper explores how drugs and environmental chemicals may cause autism by changing gene activity in brain cells.

Contribution

The paper specifically examines how certain chemicals affect epigenetic changes in neurons and glial cells related to autism.

Findings

Prenatal exposure to valproic acid or acetaminophen increases ASD risk.

Epigenetic changes in neuronal and glial cells are linked to ASD etiology.

Understanding these changes could lead to better ASD interventions.

Abstract

Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by severe deficits in social communication and interaction, repetitive movements, abnormal focusing on objects, or activity that can significantly affect the quality of life of the afflicted. Neuronal and glial cells have been implicated. It has a genetic component but can also be triggered by environmental factors or drugs. For example, prenatal exposure to valproic acid or acetaminophen, or ingestion of propionic acid, can increase the risk of ASD. Recently, epigenetic influences on ASD have come to the forefront of investigations on the etiology, prevention, and treatment of this disorder. Epigenetics refers to DNA modifications that alter gene expression without making any changes to the DNA sequence. Although an increasing number of pharmaceuticals and environmental chemicals are being implicated in the etiology of ASD, here, we specifically focus on the molecular influences of the abovementioned chemicals on epigenetic alterations in neuronal and glial cells and their potential connection to ASD. We conclude that a better understanding of these phenomena can lead to more effective interventions in ASD.

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