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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

NEUROINFLAMAÇÃO E VIA APOPTÓTICA NA EPILEPSIA / NEUROINFLAMMATION AND APOPTOTIC PATHWAY IN EPILEPSY

Kegler, Aline 09 February 2015 (has links)
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior / Epilepsy is a neurological disease that affects around 1% of world population, with neurobiological, neurochemical, cognitive and psychological consequences. Despite the good prognosis, the high number of epilepsy patients who have refractory seizures to medicine, reflects lack of a better understanding about excitotoxic disorders characteristic of the disease. So, the aim of the study was to investigate if there is an association between apoptotic markers and inflammation pathway in epileptic subjects and those without the disease. Blood samples were collected from subjects with epilepsy and were measured protein carbonyl, tumor necrosis factor alpha (TNF-α), interferon gamma (IFN-لا), acetylcholinesterase (AChE), caspases (CASP8 and CASP3) and picogreen (PG). The results showed an increase in all analyzed biochemistry parameters from epilepsy subjects when compared to healthy, suggesting that there is a relation between this disease with apoptotic and inflammatory markers. Furthermore, there was a positive correlation between TNF-α with CASP 8 and 3. IFN-لا was just correlated with caspase 3. The correlation between analyzed parameters with seizure severity and antiepileptic drugs (AEDs) treatment was not significant, indicating that medicine administration and symptoms improve did not influence obtained results. So, our results suggest that epileptic seizures can induce the creation of a vicious circle between neuroinflammation and cell death, resulting in DNA damage in epilepsy patients. Furthermore, we suggest that AEDs acting in TNF-α or IFN-لا pathway could represent an adjunctive therapy in epilepsy patients treatment. / A epilepsia é uma doença neurológica que afeta em torno de 1% da população mundial, tendo consequências no âmbito neurobiológico, neuroquímico, cognitivo e psicológico. Apesar do bom prognóstico, o elevado número de pacientes com epilepsia, que apresentam convulsões refratárias aos medicamentos, reflete a falta de um melhor entendimento dos distúrbios excitotóxicos característicos desta doença. A partir disto, o objetivo deste estudo foi investigar se existe uma associação entre os marcadores apoptóticos e a via inflamatória em indivíduos epilépticos e naqueles sem a doença. Amostras de sangue foram coletadas de pacientes com epilepsia e posteriormente foram analisados os níveis de proteína carbonil, fator de necrose tumoral alfa (TNF-α), interferon gama (INF-لا), acetilcolinesterase (AChE), caspases (CASP8 e CASP3) e picogreen (PG). Os resultados mostraram um aumento em todos os parâmetros bioquímicos analisados no sangue de pacientes com epilepsia quando comparado aos controles. Além disso, foi observada uma correlação positiva entre TNF-α com as caspases (8 e 3). O IFN-لا correlacionou-se apenas com os níveis da caspase 3. A correlação entre os parâmetros analisados com a gravidade das crises epilépticas e o tratamento com fármacos antiepilépticos (FAEs) não foi significativa, indicando que a administração de medicamentos para controle das crises e melhora dos sintomas não influenciou nos resultados obtidos. Dessa forma, os nossos dados sugerem que as crises epilépticas podem induzir a geração de um ciclo vicioso entre neuroinflamação e apoptose celular, induzindo ao estresse oxidativo e resultando no dano ao DNA nos pacientes com epilepsia. Além disso, nós sugerimos que o uso de FAEs que atuem na via do TNF-α ou IFN-لا poderia representar uma terapia complementar no tratamento dos pacientes epilépticos.

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