Neuroinflammation in Acquired Epilepsy

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Background

As one of the most prevalent neurological disorders, epilepsy affects about 65 million people worldwide. The past two decades has witnessed marked scientific advances in understanding seizure initiation and propagation following brain insults, such as de novo status epilepticus (SE), traumatic brain injuries (TBIs), CNS infections, brain tumors; strokes, etc. However, there are still over one-third of epilepsy patients who suffer seizures that are resistant to current frontline medications. Unfortunately all current anti-seizure drugs (ASDs) act merely to suppress seizures in patients who have already been diagnosed with epilepsy and at the moment there is no US FDA-approved medical treatment that can prevent the development of epilepsy in people at risk or modify the seizure progression in those who have epilepsy. The mechanisms that transform a normal brain to one with epilepsy (i.e., epileptogenesis) are therefore likely to be quite different to those that drive seizures in the epileptic brain. Discovery of strategies to prevent epilepsy and/or suppress its expression once developed must hinge on understanding of signaling pathways that trigger epileptogenic processes, which accumulate in the occurrence of unprovoked seizures, i.e., epilepsy.

Many Mendelian forms of epilepsy involve ion channel mutations, and most current ASDs suppress seizures via directly modulating various ion channels. However, for acquired forms of epilepsy we must seek cellular and molecular mechanisms that cause deregulations of ion channels. In so doing we might be able to identify epileptogenic mediators that dictate the expression and/or functional state of ion channels that set the seizure threshold. Evidence from clinical and pre-clinical studies over the past two decades supports that a number of key proinflammatory mediators can induce acquired channelopathies either directly through their neuronal receptors or indirectly via receptors on glial cells, which, in turn, release neuromodulatory factors. Modulation of these proinflammatory mediators might hold keys to interrupting epileptogenic processes and provide prevention and/or modification strategies for acquired epilepsy.

This research topic aims to further elucidate how proinflammatory mediators trigger and/or facilitate the epileptogenic processes including the disruption of blood-brain barrier (BBB), neuronal death, reactive gliosis, neuronal plasticity, etc., thereby leading to unprovoked epileptic seizures. We welcome authors to submit both Original Research and Review articles, covering, but not limited to the following subtopics:
• New animal models for various acquired forms of epilepsy
• Novel pharmacotherapies for acute and epileptic seizures
• Alterations of neuroinflammatory mediators by seizure-precipitating insults
• Similarities and differences of inflammation in different forms of acquired epilepsy
• Functions of microglia and astrocytes in the epileptic brain
• Regulations of BBB permeability during acquired epileptogenesis
• Proinflammatory mediators as targets for pharmacoresistant epilepsy
• Modulating key inflammatory pathways to interrupt epileptogenesis
• Neuroinflammation in behavioral comorbidities associated with epilepsy

Keywords: astrogliosis, blood-brain barrier, brain tumor, CNS infection, epileptogenesis, microgliosis, neuronal death, post-stroke epilepsy, status epilepticus, traumatic brain injury

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