The role of inflammation in the development of epilepsy
- PMID: 29764485
- PMCID: PMC5952578
- DOI: 10.1186/s12974-018-1192-7
The role of inflammation in the development of epilepsy
Abstract
Epilepsy, a neurological disease characterized by recurrent seizures, is often associated with a history of previous lesions in the nervous system. Impaired regulation of the activation and resolution of inflammatory cells and molecules in the injured neuronal tissue is a critical factor to the development of epilepsy. However, it is still unclear as to how that unbalanced regulation of inflammation contributes to epilepsy. Therefore, one of the goals in epilepsy research is to identify and elucidate the interconnected inflammatory pathways in systemic and neurological disorders that may further develop epilepsy progression. In this paper, inflammatory molecules, in neurological and systemic disorders (rheumatoid arthritis, Crohn's, Type I Diabetes, etc.) that could contribute to epilepsy development, are reviewed.Understanding the neurobiology of inflammation in epileptogenesis will contribute to the development of new biomarkers for better screening of patients at risk for epilepsy and new therapeutic targets for both prophylaxis and treatment of epilepsy.
Keywords: Blood–brain barrier (BBB) breakdown; Epileptogenesis; Inflammation; Neurological disorders; Systemic inflammatory disorders.
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References
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- Laxer K, Trinka E, Hirsch L, et al. The consequences of refractory epilepsy and its treatment. Epilepsy Behav. 2014;37:59–70. - PubMed
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- Musto A, Gjorstrup P, Bazan N. The omega-3 fatty acid-derived neuroprotectin D1 limits hippocampal hyperexcitability and seizure susceptibility in kindling epileptogenesis. Epilepsia. 2011;52(9):1601–1608. - PubMed
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