Valproic acid (VPA), which is an anticonvulsant and mood stabiliser, has been applied in the treatment of a number of neurological and psychiatric conditions. However, there are severe neurotoxic side effects that result from its use, especially when taken at certain developmental stages of a child’s brain. Consequently, the present narrative review aimed at not only summarising what is presently known about the neurotoxicity of VPA and the related neuropsychiatric disorders but also focused on potential interventions. Most of the neurotoxic effects of VPA are due to its ability to elucidate the production of reactive oxygen species, cause mitochondrial dysfunction, and epigenetics. It also facilitates neuronal damage by distorting the excitatory and inhibitory neurotransmission, increasing the excitotoxicity, oxidative stress, and mitochondrial dysfunction. These neurotoxic mechanisms are strongly associated with multiple neurodevelopmental disorders. As an example, prenatal VPA use is one of the common risk factors in autism spectrum disorder (ASD) that is correlated with complex social and communication deficits. VPA, which is used to treat epilepsy, may paradoxically increase seizure propensity by affecting neuronal excitability and synaptic input. Understanding these pathways can help to decrease the neurotoxicity of VPA without decreasing its drug efficacy in sensitised children.
نوع مطالعه:
Review |
موضوع مقاله:
Cellular and molecular Neuroscience دریافت: 1403/10/28 | پذیرش: 1404/9/1 | انتشار: 1404/10/30