Molecular cascades that mediate the influence of inflammation on epilepsy

被引：118
作者：
Friedman, Alon [1 ]
Dingledine, Ray [2 ]
机构：
[1] Ben Gurion Univ Negev, Fac Hlth Sci, Dept Physiol & Neurobiol, Zlotowski Ctr Neurosci, Beer Sheva, Israel
[2] Emory Univ, Dept Pharmacol, Emory Chem Biol Discovery Ctr, Atlanta, GA 30322 USA
来源：
EPILEPSIA | 2011年 / 52卷
关键词：
Blood-brain barrier; Cytokines; Epileptogenesis; Immune; BLOOD-BRAIN-BARRIER; TEMPORAL-LOBE EPILEPSY; EXPERIMENTAL FEBRILE SEIZURES; NECROSIS-FACTOR-ALPHA; ENHANCES EPILEPTOGENESIS; EPILEPTIFORM ACTIVITY; P-GLYCOPROTEIN; UP-REGULATION; RAT-BRAIN; IN-VITRO;
D O I：
10.1111/j.1528-1167.2011.03034.x
中图分类号：
R74 [神经病学与精神病学];
学科分类号：
摘要：
P>Experimental evidence strongly indicates a significant role for inflammatory and immune mediators in initiation of seizures and epileptogenesis. Here we will summarize data supporting the involvement of IL-1 beta, TNF-alpha and toll-like receptor 4 in seizure generation and the process of epileptogenesis. The physiological homeostasis and control over brain immune response depends on the integrity of the blood-brain barrier, transforming growth factor (TGF)-beta signaling and leukocyte migration. To what extent targeting the immune system is successful in preventing epileptogenesis, and which signaling pathway should be beleaguered is still under intensive research.
引用
收藏
页码：33 / 39
页数：7
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