Publicação
The role of brain derived neurotrophic factor (BDNF) on epilepsy
| Resumo: | Epilepsy is commonly defined as a condition of chronic predisposition for seizures. Importantly, none of the “antiepileptic dugs” used in clinical practice can prevent the development of epilepsy after an epileptic insult, and thus are increasingly referred as anti-seizure drugs rather than anti-epileptic. Together with the fact that about 50% of treated patients continue to experience seizures, the pharmacological intervention is far from the ideal, and consequently the need for new therapeutic alternatives emerges. Although controversial, the modulation of neurotrophin signaling, in particular of the brain-derived neurotrophic factor (BDNF), has been seen as promising therapeutic strategy. The present review aims to compile the available data related to the role of the BDNF signaling on epilepsy and the possible mechanisms involved such as modulation of excitatory and inhibitory neuronal transmission; mossy fiber sprouting, and neuropeptide Y. Taken together the presented data clear show a discrepancy among the available data. This could be related to differences in the 1) animal model; 2) induction of spontaneous recurrent seizures protocol 3) schedule of exogenous BDNF administration; 4) genetic models of BDNF signaling modulation. More studies are needed to unveil the role of this neurotrophin upon epilepsy and whether the modulation of its signaling pathways could be considered a therapeutic strategy. |
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| Autores principais: | Guimarães, Diogo Filipe Andrade |
| Assunto: | Neurotrofinas Fator neurotrófico derivado do cérebro (BDNF) TrkB Recetores A2A da adenosina NMDA Epilepsia |
| Ano: | 2016 |
| País: | Portugal |
| Tipo de documento: | dissertação de mestrado |
| Tipo de acesso: | acesso aberto |
| Instituição associada: | Universidade de Lisboa |
| Idioma: | inglês |
| Origem: | Repositório da Universidade de Lisboa |
| Resumo: | Epilepsy is commonly defined as a condition of chronic predisposition for seizures. Importantly, none of the “antiepileptic dugs” used in clinical practice can prevent the development of epilepsy after an epileptic insult, and thus are increasingly referred as anti-seizure drugs rather than anti-epileptic. Together with the fact that about 50% of treated patients continue to experience seizures, the pharmacological intervention is far from the ideal, and consequently the need for new therapeutic alternatives emerges. Although controversial, the modulation of neurotrophin signaling, in particular of the brain-derived neurotrophic factor (BDNF), has been seen as promising therapeutic strategy. The present review aims to compile the available data related to the role of the BDNF signaling on epilepsy and the possible mechanisms involved such as modulation of excitatory and inhibitory neuronal transmission; mossy fiber sprouting, and neuropeptide Y. Taken together the presented data clear show a discrepancy among the available data. This could be related to differences in the 1) animal model; 2) induction of spontaneous recurrent seizures protocol 3) schedule of exogenous BDNF administration; 4) genetic models of BDNF signaling modulation. More studies are needed to unveil the role of this neurotrophin upon epilepsy and whether the modulation of its signaling pathways could be considered a therapeutic strategy. |
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