Վալպրոյաթթուն՝ Աուտիզմի Սպեկտրի Խանգարումների Մոդելավորման Մեջ

Abstract

Autism spectrum disorders (ASD) are neurodevelopmental disorders, characterized by impaired social interaction, repetitive behaviors, and restricted interests. The global prevalence of autism is approximately 1 in 100, with an increasing trend, particularly in North America, where it has reached 1 in 44. Despite extensive research, ASD’s pathogenesis remains unclear, though genetic, epigenetic, and environmental factors play key roles. In ASD animal models, such as those induced with valproic acid (VPA), researchers study ASD’s molecular, biochemical, and behavioral alterations. VPA, an antiepileptic drug with histone deacetylase inhibition properties, influences epigenetic regulation, leading to synaptic and neural development changes that resemble ASD traits in humans. Research highlights VPA’s effects on oxidative stress and synaptic changes, including impacts on proteins like VGAT and reductions in inhibitory synaptic transmission. Studies also suggest that antioxidants like astaxanthin may improve ASD-related behavioral symptoms in these models. This article aims to review synaptic changes in VPA-induced ASD models, with a focus on the role of VPA-induced oxidative stress and histone acetylation alterations. These findings offer insights into ASD pathogenesis, providing a foundation for exploring novel therapeutic approaches to mitigate ASD risks and improve treatment outcomes.