Epilepsy affects approximately 1% of world population. Approximately 40% of all epilepsy cases are "Acquired Epilepsy" due to a brain injury. The process by which a healthy brain with a balance between excitation and inhibition gets transformed into a hyperexcitable circuit of neurons is known as epileptogenesis. By understanding molecular mechanisms that participate in epileptogenesis, we can develop insight into new therapeutic targets to halt its progression.
Our research has shown that neuronal calcium increases significantly following brain injuries including status epilepticus, or traumatic brain injury. A significant "calcium plateau" is maintained during epileptogenesis. As an important second messenger, sustained elevations in calcium can have tremendous implications on neuronal plasticity, gene expression, behavioral co-morbidities, and the ultimate expression of epilepsy.
Current efforts are aimed at further understanding changes in expression/activity of various regulators of cellular calcium following brain injury. This knowledge may provide new therapeutic targets through which we are able to lower neuronal calcium post-injury and, perhaps in doing so, prevent the development of Acquired Epilepsy and associated morbidities.