Targeting epigenetic dysregulation in autism spectrum disorders.

Both genetic and environmental factors can disturb the epigenome, influencing autism spectrum disorders (ASD) development and underlying the heterogenic complexity of autistic phenotypes. A U-shaped curve links the autistic phenotype with genetically and environmentally induced epigenomic imbalance. Analysis of DNA methylation in peripheral tissues can provide biomarkers valuable for diagnosing both idiopathic and syndromic ASD. Human iPSC-derived neurons and cerebral organoids (COs) replicate ASD epigenetic signatures and provide a platform for drug testing, personalized medicine, and regenerative therapies. Advances in our capacity to manipulate the neural epigenome using epidrugs and epi-editing approaches may yield novel therapeutic approaches to treat ASD. Autism spectrum disorders (ASD) comprise a range of neurodevelopmental pathologies characterized by deficits in social interaction and repetitive behaviors, collectively affecting almost 1% of the worldwide population. Deciphering the etiology of ASD has proven challenging due to the intricate interplay of genetic and environmental factors and the variety of molecular pathways affected. Epigenomic alterations have emerged as key players in ASD etiology. Their research has led to the identification of biomarkers for diagnosis and pinpointed specific gene targets for therapeutic interventions. This review examines the role of epigenetic alterations, resulting from both genetic and environmental influences, as a central causative factor in ASD, delving into its contribution to pathogenesis and treatment strategies. [ABSTRACT FROM AUTHOR]