4.5 Review

Leukocyte trafficking mechanisms in epilepsy

Journal

MOLECULAR IMMUNOLOGY
Volume 55, Issue 1, Pages 100-104

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.molimm.2012.12.009

Keywords

Leukocyte trafficking; Epilepsy; Seizures; Inflammation; Adhesion molecules; Chemokines

Funding

  1. European Research Council [261079- NEUROTRAFFICKING]
  2. National Multiple Sclerosis Society (NMSS), New York, NY, USA
  3. Fondazione Italiana Sclerosi Multipla (FISM)
  4. Associazione Italiana per la Ricerca sul Cancro (AIRC) [IG 8690]
  5. Ricerca Finalizzata Project, Italian Ministry of Health
  6. Ministry of Education and Research (MIUR)
  7. Fondazione Cariverona

Ask authors/readers for more resources

Epilepsy is a chronic disorder that affects 1% of the world population and is characterized by chronically reoccurring seizures. Seizures are initiated by abnormal excessive or synchronous neuronal activity in the brain. Epilepsy requires life long anti-convulsant therapy and current therapies for epilepsy selectively target neuronal activity. In the last decade, cytokines and vascular alterations have been discussed in relation to the pathogenesis of epilepsy, suggesting a potential role for inflammation mechanisms in seizure induction. More recently, it has been shown that leukocyte trafficking plays a key role in seizure generation, and that anti-leukocyte adhesion therapy has therapeutic and preventative effects in an experimental model of human epilepsy. These results were supported by evidence in humans showing that leukocytes accumulate in the brain parenchyma of patients with different types of epilepsy. Finally, recent clinical observations suggest that therapies able to interfere with leukocyte trafficking may have a therapeutic effect in epilepsy. The emerging role for leukocytes and leukocyte adhesion mechanisms in seizure generation provides insight into the mechanisms of brain damage and may contribute to the development of novel therapeutic strategies in epilepsy. (C) 2012 Elsevier Ltd. All rights reserved.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.5
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available