Introdução: A doença de Parkinson (DP) apresenta etiologia multifatorial, que inclui disfunções genéticas e ambientais. Resulta da perda progressiva de células produtoras de dopamina na substância negra e do acúmulo de proteínas, principalmente a alfa-sinucleína (SNCA), nos corpos de Lewy. Esses aspectos levam a sintomatologia de bradicinesia, tremor de repouso e rigidez. Neurônios dopaminérgicos necessitam de demanda energética, assim, distúrbios mitocondriais, como bioenergéticos, mutações no DNA nuclear ou mitocondrial, alterações no transporte, movimento e morfologia dessa organela, estão associados à DP. Objetivo: Esclarecer a relação de distúrbios mitocondriais e o desenvolvimento da DP. Materiais e Métodos: Revisão bibliográfica da literatura realizada na bases de dados PubMed/MEDLINE, durante abril e maio de 2021, por meio do cruzamento dos descritores, cadastradas no DeCS, “Parkinson Disease” AND “Mitochondria”. Foram incluídos artigos com textos disponíveis completos gratuitamente, publicados nos últimos cinco anos, em inglês e português, com o estudo envolvendo humanos e excluídos aqueles cujo título ou resumo eram incoerentes com a linha de interesse da atual revisão. Com base nisso, encontraram-se 106 artigos, dos quais 8 foram selecionados, além de outros 2 e um livro didático, julgados importantes para a discussão do tema. Resultados: Evidências científicas mostram que mutações nos genes SNCA, LRRK2, Parkin e PINK1 implicam em mecanismos mitocondriais deficitários que desenvolvem a DP. A mutação do gene SNCA sensibiliza neurônios ao estresse oxidativo e provoca danos por toxinas, o que induz a fragmentação mitocondrial e a produção de radicais livres. A PARKIN previne o edema e a ruptura mitocondrial secundária à toxicidade, ou seja, relaciona-se à integridade mitocondrial. Alterações na proteína PINK1 interferem no potencial da membrana mitocondrial. Ademais, mutações na quinase LRRK2 interferem no tráfego mitocondrial e nas proteínas da membrana externa. Logo, modificações nesses genes além de diminuírem a atividade do complexo I da cadeia transportadora de elétrons, prejudicam a produção energética, a regulação da síntese de dopamina e sua neurotransmissão. Conclusão: De acordo com a literatura, observa-se a fundamental relação entre DP e disfunções mitocondriais, todavia mais estudos são necessários para esclarecer e justificar tal abordagem, como forma de melhorar o prognóstico e a terapêutica.
Publicado
2021-09-10
Como Citar
Zamprogno, N. P. ., & Novaes, M. A. S. . (2021). REVISÃO: DOENÇA DE PARKINSON E SUAS ETIOLOGIAS MITOCONDRIAIS. Revista Multidisciplinar Em Saúde, 2(3), 15. https://doi.org/10.51161/rems/1956
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