:
Retinoic acid, a metabolite of vitamin A, acts through either genomic or nongenomic actions. The genomic action of
retinoids exerts effects on gene transcription through interaction with retinoid receptors such as retinoic acid receptors (RARα,
β, and γ) and retinoid X receptors (RXRα, β, and γ) that are primarily concentrated in amygdala, pre-frontal cortex, and
hippocampal areas in the brain. In response to retinoid binding, RAR/RXR heterodimers undergo major conformational changes
and orchestrate the transcription of specific gene networks. Previous experimental studies have reported that retinoic acid exerts
an antiepileptogenic effect through diverse mechanisms, including the modulation of gap junctions, neurotransmitters, long-term
potentiation, calcium channels and some genes. To our knowledge, there are no previous or current clinical trials evaluating the
use of retinoic acid for seizure control.