2025/12/16 by Harshit Shringi, Muskan Tomar · 1 voice
Medicine · Neuroscience · #Epilepsy research and treatment #Neuroscience and Neuropharmacology Research #Tryptophan and brain disorders
paper · doi:10.70389/pjs.100192
openalex publication_date 2025/12/16 · openalex created_date 2025/12/20 · openalex updated_date 2026/06/11
Epilepsy is a persistent neurological condition defined by recurring, unprovoked seizures due to irregular neuronal coordination and impaired communication of neural circuits. Recent studies have indicated that the dysfunction of neural networks in epilepsy extends beyond hyperexcitability and includes maladaptive processes involving neuronal connectivity, glial signalling, and synaptic plasticity. The effects observed here are fundamentally driven by a cluster of pathophysiological changes involving oxidative stress, neuroinflammation, and mitochondrial derangements. Disruption of redox balance leads to increased production of reactive oxygen species that damage neuronal membranes while that trigger maladaptive alteration of neurotransmitters. Inflammatory molecules IL-1β, TNF-α, and NF-κB similarly deregulate synaptic efficacy and lead to excitotoxic cascades. This review aims to pull together our current understanding of molecular and cellular mechanisms that sustain dysfunction of neural networks and how molecular and cellular mechanisms can inform therapeutic interventions. Recent advances in antioxidant and anti-inflammatory drug development, nanocarrier-based biotechnology and drug delivery, gene therapy, or delivery of neuroprotective plant-based chemicals offer potentially promising directions, and show satisfactory evidence towards the goal of restoring network function. By establishing nexus for mechanistic understanding and translating that to implementation, our review will articulate a new potential for investigating precision-based, multi-targeted therapeutic interventions which can have impact upon seizure control and can maximise neuroprotection in epilepsy.