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Advisor(s)
Abstract(s)
Introdução: A pandemia causada pelo vírus SARS-CoV-2 trouxe muitos desafios para a
população geral e para a comunidade científica. O vírus causou durante dois anos cerca de
753.479.439 casos e 6.812.798 mortes, segundo os dados da OMS. Os casos apresentavam
diferentes graus de severidade da doença, desde assintomáticos a quadros clínicos severos
com eventual morte. Com o aumento dos casos da covid-19, verificou-se que a infeção pelo
vírus SARS-CoV-2 levava à incidência de inúmeras patologias relacionadas com o sistema
nervoso. Desde sintomas ligeiros até efeitos trombóticos cerebrais relevantes com impacto
na qualidade de vida. Nesta dissertação de mestrado pretende-se verificar se existe uma
relação direta entre o vírus SARS-CoV-2 e o sistema nervoso e compreender as bases
fisiopatológicas de algumas das sintomatologias e doenças neurológicas apresentadas no
decurso da doença e após a sua resolução.
Metodologia: Pesquisa bibliográfica em plataformas online com análise de artigos entre
2020 e 2023.
Resultados: O vírus através da ACE2 infeta as células que a expressam, as células
endoteliais cerebrais, os neurónios, as células gliais e os astrócitos. Para além disso, a
inflamação sistémica, com libertação de citocinas e ativação das células do sistema
imunitário cerebral levam à neuroinflamação. A neuroinflamação é a base de inúmeras das
patologias apresentadas na covid-19, desde cefaleias, convulsões, encefalites e
encefalopatias. Para além disso, o estado pró-inflamatório contribui para coagulopatias com
desfechos menos favoráveis ou com o desenvolvimento de microtrombos afetando o normal
funcionamento cerebral. O neurotropismo do vírus, pela ligação direta a ACE2, está
envolvida nas alterações do olfato e paladar e pode levar à SDRA. Na PASC verificamos que
um dos mecanismos envolvidos é a inflamação crónica, com aumento da secreção de
interferões e citocinas diferentes das da fase aguda, levando a uma desregulação do circuito
inibitório GABA, afetando os inúmeros domínios cognitivos, principalmente a função
executiva e a memória de curto prazo.
Conclusão: Concluímos que o vírus SARS-CoV-2 tem relação com o sistema nervoso e os
principais mecanismos subjacentes ao desenvolvimento destes distúrbios neurológicos são:
através da ligação direta do vírus com a ACE2 e a neuroinflamação. Estes dois mecanismos
são a base subjacente dos vários distúrbios neurológicos encontrados na doença covid-19.
Introduction: The pandemic caused by the SARS-CoV-2 virus brought several challenges for the general population and for the scientific comunity. The virus caused about 753.479.439 cases and 6.812.798 deaths over two years, according to WHO data. The cases of covid-19 had different grades of severity, ranging from asymtomatic disease to critical stage evolving death outcome. With the increase of cases of covid-19 around the world, it was clear that the virus SARS-CoV-2 also caused several patologies related to the nervous system, from mild symptoms to relevant trombotic effects on the brain with impact in the quality of life. In this master’s thesis, it is intended to verify if there is a direct correlation between the SARS-CoV-2 virus and the nervous system, and to understand the pathophysiological bases of some of the neurologic sintomatology and diseases present during the disease and after its resolution. Methodology: Bibliographic research on online platforms with analysis of articles between 2020 and 2023. Results: The virus through the ACE2 infect the cells that express it, the brain endotelial cells, neurons, glial cells and astrocytes. Futhermore, the systemic inflammation with release of cytokines and activation of brain imune system cells leads to neuroinflammation. Neuroinflammation is the basis of many of the neurologic pathologies presented in covid19, from headaches, seizures, encephalitis and encephalopathies. In addition, the proinflammatory state contribute to coagulophaties, with less favorable outcome or the development of microthrombi affecting normal brain functioning. The neurotropism of SARS-CoV-2, through direct binding to ACE2, is involved in changes of smell and taste and can lead to ARDS. In PASC we verified that one of the mecanism involved is chronic inflammation, with increased secretion of interferons and cytokines different from those of the acute phase, leading to the dysregulation of GABA inhibitory circuit, affecting numerous cognitive domains, manly the executive function and short-term memory. Conclusion: We come to the conclusion that the SARS-CoV-2 virus has a relation with the nervous system and the main mecanisms underlying the development of these neurological disorders are: through the direct connection of the virus with ACE2 and neuroinflammation. These mecanisms are the pathophisiological bases of many disorders developed in the context of covid-19 disease.
Introduction: The pandemic caused by the SARS-CoV-2 virus brought several challenges for the general population and for the scientific comunity. The virus caused about 753.479.439 cases and 6.812.798 deaths over two years, according to WHO data. The cases of covid-19 had different grades of severity, ranging from asymtomatic disease to critical stage evolving death outcome. With the increase of cases of covid-19 around the world, it was clear that the virus SARS-CoV-2 also caused several patologies related to the nervous system, from mild symptoms to relevant trombotic effects on the brain with impact in the quality of life. In this master’s thesis, it is intended to verify if there is a direct correlation between the SARS-CoV-2 virus and the nervous system, and to understand the pathophysiological bases of some of the neurologic sintomatology and diseases present during the disease and after its resolution. Methodology: Bibliographic research on online platforms with analysis of articles between 2020 and 2023. Results: The virus through the ACE2 infect the cells that express it, the brain endotelial cells, neurons, glial cells and astrocytes. Futhermore, the systemic inflammation with release of cytokines and activation of brain imune system cells leads to neuroinflammation. Neuroinflammation is the basis of many of the neurologic pathologies presented in covid19, from headaches, seizures, encephalitis and encephalopathies. In addition, the proinflammatory state contribute to coagulophaties, with less favorable outcome or the development of microthrombi affecting normal brain functioning. The neurotropism of SARS-CoV-2, through direct binding to ACE2, is involved in changes of smell and taste and can lead to ARDS. In PASC we verified that one of the mecanism involved is chronic inflammation, with increased secretion of interferons and cytokines different from those of the acute phase, leading to the dysregulation of GABA inhibitory circuit, affecting numerous cognitive domains, manly the executive function and short-term memory. Conclusion: We come to the conclusion that the SARS-CoV-2 virus has a relation with the nervous system and the main mecanisms underlying the development of these neurological disorders are: through the direct connection of the virus with ACE2 and neuroinflammation. These mecanisms are the pathophisiological bases of many disorders developed in the context of covid-19 disease.
Description
Keywords
Déficits Cognitivos Neuroinflamação e Sintomas Neurológicos Neurotropismo Sistema Nervoso