Many different neurobiological processes have been implicated as potential targets for antiepileptogenic or disease-modifying therapies.
These processes include accumulation of neurodegenerative proteins (such as human tau and β-amyloid), neurogenesis, pro-inflammatory processes (such as interleukin 1β, transforming growth factor β and activin receptor-like kinase), changes in neuronal voltage and ligand gated ion channels, neurotransmitter release or uptake characteristics, and intracellular signalling cascades (such as brain-derived neurotrophic factor and tropomyosin receptor kinase, the mechanistic target of rapamycin [mTOR] pathway, adenosine/adenosine kinase, and microglia activation)
Many of these processes are thought to be driven by epigenomic changes induced by the epileptogenic insult. Which, if any, of these processes are fundamental to epileptogenesis is still to be established and there is no clinically validated antiepileptogenic therapy.