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The Role of JNK Pathway in the Process of Excitotoxicity Induced by Epilepsy and Neurodegeneration

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Pharmacoresistance in Epilepsy

Abstract

The c-Jun N-terminal kinases (JNKs) are members of the MAPK family and can be activated in neurons by different neurotoxins such as kainic acid (an experimental model of epilepsy), beta amyloid, and nitropropionic acid. Although JNKs have different physiological functions they have been linked mainly to the apoptotic process in neurons and other cell types. Therefore, the JNK signaling pathway constitutes an important target to prevent the apoptotic cell death in epilepsy and neurodegeneration. In the present chapter, the role of JNKs, specifically the JNK3 isoform, as a potential target for epilepsy and neurodegenerative diseases will be discussed. In addition, the pharmacological compounds that inhibit the JNKs signaling pathway constitutes a potential therapeutic intervention to prevent neuronal death.

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Acknowledgements

This study was funded by grant 2009/SGR00853 from the Generalitat de Catalunya (autonomous government of Catalonia), grants BFU2010-19119/BFI, SAF2011-­23631, and SAF2009-13093 from the Spanish Ministerio de Ciencia e Innovación, grant PI080400 and PS09/01789 from the Instituto de Salud Carlos III, and grant 610RT0405 from Programa Iberoamericano de Ciencia y Tecnologia para el Desarrollo (CYTED).

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Correspondence to Antoni Camins Espuny .

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Auladell, C. et al. (2013). The Role of JNK Pathway in the Process of Excitotoxicity Induced by Epilepsy and Neurodegeneration. In: Rocha, L., Cavalheiro, E. (eds) Pharmacoresistance in Epilepsy. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-6464-8_7

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