====== Epileptogenesis ======

In a mechanistic context, epileptogenesis is the process by which a brain network that was previously normal is functionally altered toward increased seizure susceptibility, thus having an enhanced probability to generate spontaneous recurrent seizures (SRSs).
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[[Photosensitive epilepsy]].
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A variety of neuropeptides play important roles as [[neurotransmitter]]s or neurotransmitter modifiers in the brain, and may be involved in the incidence and development of epilepsy. In recent years, the following neuropeptides: [[galanin]] (GAL), [[neuropeptide Y]] (NPY), [[neuropeptide]] [[substance P]] (SP), [[cholecystokinin]] (CCK), as well as wake-promoting neuropeptide (ORE) have been discovered to be closely associated with [[epilepsy]]
((Gao JB, Bao M. Plasma neuropeptide as a prognostic marker of vagus nerve
stimulation in the treatment of epilepsy. Brain Stimul. 2020 Apr 1;13(4):959-960.
doi: 10.1016/j.brs.2020.03.021. [Epub ahead of print] PubMed PMID: 32380447.
)).
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Maladaptive epigenetic changes, which include [[methylation]] of DNA and [[acetylation]] of histones - among other mechanisms, are now well recognized to play a functional role in the development of epilepsy and its progression. The methylation hypothesis of epileptogenesis suggests that changes in
[[DNA methylation]] are implicated in the progression of the disease. In this context, global DNA hypermethylation is particularly associated with chronic epilepsy. Likewise, acetylation changes of histones have been linked to epilepsy development. Clinical as well as experimental evidence demonstrates that epilepsy and its progression can be prevented by metabolic and biochemical manipulations that target previously unrecognized epigenetic functions contributing to epilepsy development and maintenance of the epileptic state. 
A review of Boison discusses epigenetic mechanisms implicated in epilepsy development as well as metabolic and biochemical interactions thought to drive epileptogenesis. Therefore, metabolic and biochemical mechanisms are identified as novel targets for epilepsy prevention. They specifically discussed [[adenosine]] biochemistry as a novel therapeutic strategy to reconstruct the DNA methylome as an antiepileptogenic strategy as well as metabolic mediators, such as beta-hydroxybutyrate, which affect histone acetylation. Finally, metabolic dietary interventions (such as the [[ketogenic diet]]) which have the unique potential to prevent epileptogenesis through recently identified epigenetic mechanisms will be reviewed
((Boison D, Rho JM. Epigenetics and epilepsy prevention: the therapeutic
potential of adenosine and metabolic therapies. Neuropharmacology. 2019 Aug
13:107741. doi: 10.1016/j.neuropharm.2019.107741. [Epub ahead of print] Review.
PubMed PMID: 31419398.
)).
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Studies have shown that [[microRNA]]s play a role in the development of [[epilepsy]] by regulating downstream target [[Messenger RNA]]. 

[[Traumatic brain injury]] (TBI) and [[status epilepticus]] (SE) have both been linked to the development of human [[epilepsy]]. Although distinct etiologies, [[research]] has suggested the convergence of molecular mechanisms underlying [[epileptogenesis]] following these [[insult]]s. One such mechanism involves the neurotrophin brain-derived neurotrophic factor ([[BDNF]]) and its high-affinity receptor, [[tropomyosin receptor kinase B]] (TrkB). In a review, Lin et al. focus on available data regarding the pathophysiologic role of BDNF/TrkB signaling in epilepsy development. They specifically examine the [[axonal injury]] and SE epilepsy models, two [[animal model]]s that recapitulate many aspects of TBI- and SE-induced epilepsy in humans respectively. Thereafter, they discussed aspiring strategies for targeting BDNF/TrkB signaling so as to prevent epilepsy following an insult or suppress its expression once developed
((Lin TW, Harward SC, Huang YZ, McNamara JO. Targeting BDNF/TrkB Pathways for
Preventing or Suppressing Epilepsy. Neuropharmacology. 2019 Aug 1:107734. doi:
10.1016/j.neuropharm.2019.107734. [Epub ahead of print] Review. PubMed PMID:
31377199.
)).