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Sunday, April 24, 2011

[AlternativeAnswers] The role of inflammation in epilepsy

 


The role of inflammation in epilepsy

Review

Nature Reviews Neurology 7, 31-40 (January 2011) |
doi:10.1038/nrneurol.2010.178
Subject Categories: _Epilepsy_
(http://www.nature.com/nrneurol/archive/neuro_s6_current_archive.html) | _Neuroimmunology and neuroinflammation_
(http://www.nature.com/nrneurol/archive/neuro_s19_current_archive.html) |
_Injury, repair and rehabilitation_
(http://www.nature.com/nrneurol/archive/neuro_s13_current_archive.html)
The role of inflammation in epilepsy
Annamaria Vezzani, Jacqueline French, Tamas Bartfai & Tallie Z. Baram
_About the authors_
(http://www.nature.com/nrneurol/journal/v7/n1/authors/nrneurol.2010.178.html)


(http://www.nature.com/nrneurol/journal/v7/n1/abs/nrneurol.2010.178.html?lang=en#top) Abstract
Epilepsy is the third most common chronic brain disorder, and is
characterized by an enduring predisposition to generate seizures. Despite progress
in pharmacological and surgical treatments of epilepsy, relatively little is
known about the processes leading to the generation of individual
seizures, and about the mechanisms whereby a healthy brain is rendered epileptic.
These gaps in our knowledge hamper the development of better preventive
treatments and cures for the ≈30% of epilepsy cases that prove resistant to
current therapies. Here, we focus on the rapidly growing body of evidence that
supports the involvement of inflammatory mediators—released by brain cells
and peripheral immune cells—in both the origin of individual seizures and
the epileptogenic process. We first describe aspects of brain inflammation
and immunity, before exploring the evidence from clinical and experimental
studies for a relationship between inflammation and epilepsy. Subsequently,
we discuss how seizures cause inflammation, and whether such inflammation,
in turn, influences the occurrence and severity of seizures, and
seizure-related neuronal death. Further insight into the complex role of
inflammation in the generation and exacerbation of epilepsy should yield new molecular
targets for the design of antiepileptic drugs, which might not only
inhibit the symptoms of this disorder, but also prevent or abrogate disease
pathogenesis.


(http://www.nature.com/nrneurol/journal/v7/n1/abs/nrneurol.2010.178.html?lang=en#top)

Author affiliations
A. Vezzani, J. French, T. Bartfai & T. Z. Baram
Department of Neuroscience, Mario Negri Institute for Pharmacological
Research, Via Giuseppe La Masa 19, 20156 Milan, Italy (A. Vezzani). NYU
Comprehensive Epilepsy Center, 223 East 34th Street, New York, NY 10016, USA (J.
French). Molecular and Integrative Neurosciences Department, The Scripps
Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA
(T. Bartfai). Pediatrics, Anatomy and Neurobiology, and Neurology, UC Irvine,
ZOT 4475, Irvine, CA 4475, USA (T. Z. Baram).
Correspondence to: A. Vezzani _vezzani@marionegri.it_
(mailto:vezzani@marionegri.it)
Published online 7 December 2010

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