| Title: |
Neuroinflammation in Epilepsy ; Cellular and Molecular Mechanisms |
| Authors: |
Dingledine, Ray; Varvel, Nicholas H.; Ravizza, Teresa; Vezzani, Annamaria |
| Contributors: |
Vezzani, Annamaria; Scharfman, Helen E. |
| Source: |
Jasper's Basic Mechanisms of the Epilepsies ; page 611-632 ; ISBN 0197549462 9780197549469 9780197549490 |
| Publisher Information: |
Oxford University PressNew York |
| Publication Year: |
2024 |
| Description: |
Neuroinflammation and epilepsy appear to exist in a self-reinforcing circular arrangement, whereby inflammatory pathways lower seizure threshold and the ensuing seizures trigger neuroinflammation. This forms the essential logic of anti-inflammatory therapies, which seek to interrupt the vicious cycle or to prevent it. Many if not all neuroinflammatory mediators are known to play physiological roles in the healthy brain, for example, regulation of astroglial potassium buffering by TGFβ, and the strength of excitatory synaptic transmission by PGE2 and IL-1β ανδ TNΦ. These neuromodulatory roles are usurped in epilepsy, when the neuroinflammatory mediators are transformed from their physiologic functions to agents of havoc as their local concentration rises or they persist too long in brain tissue. This chapter focuses on IL-1β, TNF, IL-6, PGE2, CXCL1, CCL2, and drivers of the complement pathway, which have all received substantial attention over the past decade. This chapter describes these inflammatory mediators and discusses how they may create a pathological milieu permissive for seizures, cell loss, and behavioral dysfunctions. |
| Document Type: |
book part |
| Language: |
English |
| ISBN: |
978-0-19-754946-9; 978-0-19-754949-0; 0-19-754946-2; 0-19-754949-7 |
| DOI: |
10.1093/med/9780197549469.003.0030 |
| Availability: |
https://doi.org/10.1093/med/9780197549469.003.0030; https://academic.oup.com/book/57972/chapter/476209150 |
| Rights: |
https://creativecommons.org/licenses/by-nc-nd/4.0/ |
| Accession Number: |
edsbas.5F4AA604 |
| Database: |
BASE |