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Campo DCValorIdioma
dc.creatorMachado, Annelisa Pimentel Rezende-
dc.creatorCarvalho, Izabella Oliveira-
dc.date.accessioned2021-12-15T14:31:18Z-
dc.date.available2021-12-15T14:31:18Z-
dc.date.issued2020-11-11-
dc.identifier.urihttps://repositorio.pucgoias.edu.br/jspui/handle/123456789/2906-
dc.description.abstractAlzheimer's disease (AD) is one of the world's leading dementias and is characterized as a progressive and chronic disorder that leads to the destruction of cholinergic neurons. The clinical picture involves a series of gradual events ranging from episodic memory loss to the outcome of memory impairment, behavior and movement performance. This paper aims to address the role of the different inflammatory mechanisms involved in the pathogenesis of Alzheimer's disease, with emphasis on the participation of innate immunity in the process of neurodegeneration. This is a narrative bibliographic review over a 12-year period (2008-2019). The databases searched were electronic data Pubmed (US National Library of Medicine) and Portal Capes, with the following descriptors "Alzheimer Disease, Inflammation, Neuroinflammation, Immunology, Cytokines". Of the 79 references obtained, 27 did not meet the inclusion criteria such as year of publication and content not related to the theme. The pathogenesis of AD is associated with the brain formation of senile plaques, which are extracellular deposits of the amyloid β peptide and intracellular neurofibrillary tangles consisting mainly of hyperphosphorylated tau protein. Astrocytes and activated microglia are characteristically found near the senile plaques, evidencing the participation of elements of the immune system in neuroinflammation and neurodegeneration. There are several factors that can activate the inflammatory pathways in AD, such as genetic mutations, environmental, emotional conditions, age and lifestyle. From such stimuli there is a cyclic process in which innate immunity cells such as microglia and astrocyte release proinflammatory molecules such as cytokines, free radicals, neurotoxins thus creating a chronic inflammatory state contributing to cell dysfunction and death with consequent progression of AD.pt_BR
dc.description.sponsorshipNão recebi financiamentopt_BR
dc.languageporpt_BR
dc.publisherPontifícia Universidade Católica de Goiáspt_BR
dc.relationRecurso dos próprios autores.pt_BR
dc.rightsAcesso Abertopt_BR
dc.subjectNeuroinflamaçãopt_BR
dc.subjectDoença de Alzheimerpt_BR
dc.subjectResposta imunept_BR
dc.subjectImunopatologiapt_BR
dc.titleNeuroinflamação na doença de Alzheimer: uma revisão da literaturapt_BR
dc.title.alternativeNeuroinflammation in Alzheimer's disease: a literature reviewpt_BR
dc.typeTrabalho de Conclusão de Cursopt_BR
dc.contributor.advisor1Rocha Sobrinho, Hermínio Maurício da-
dc.contributor.advisor1IDhttps://orcid.org/0000-0002-7521-3700pt_BR
dc.contributor.advisor1Latteshttp://lattes.cnpq.br/5573574130526137pt_BR
dc.contributor.referee1Sobrinho, Hermínio Maurício da Rocha-
dc.contributor.referee1Latteshttp://lattes.cnpq.br/5573574130526137pt_BR
dc.description.resumoA doença de Alzheimer (DA) é umas das principais demências do mundo, sendo caracterizada como uma desordem progressiva e crônica que leva a destruição de neurônios colinérgicos. O quadro clínico envolve uma série de eventos graduais desde a perda de memória episódica até o desfecho de deterioração da memória, do comportamento e da execução de movimentos. O presente artigo teve como objetivo abordar o papel dos diferentes mecanismos inflamatórios envolvidos na patogênese da doença de Alzheimer, com ênfase na participação da imunidade inata no processo de neurodegeneração. Trata-se de uma revisão bibliográfica narrativa, no período de 12 anos (2008-2019). As bases de dados para busca foram dados eletrônica Pubmed (US National Library of Medicine) e Portal Capes, com os seguintes descritores “Alzheimer Disease, Inflammation, Neuroinflammation, Immunology, Cytokines”. Das 79 referências obtidas, 27 não apresentaram os critérios de inclusão como o ano da publicação e conteúdo não relacionado ao tema. A patogenia da DA associa-se à formação cerebral das placas senis, que são depósitos extracelulares do peptídeo β amiloide e emaranhados neurofibrilares intracelulares constituídos principalmente por proteína tau hiperfosforilada. Astrócitos e micróglias ativados são caracteristicamente encontrados próximos às placas senis, evidenciado a participação de elementos do sistema imune na neuroinflamação e neurodegeneração. Vários são os fatores capazes de ativar as vias inflamatórias na DA, como mutações genéticas, condições ambientais, emocionais, idade e hábitos de vida. A partir de tais estímulos há um processo cíclico em que células da imunidade inata como a micróglia e o astrócito liberam moléculas pró-inflamatórias como citocinas, radicais livres, neurotoxinas criando assim um estado inflamatório crônico contribuindo para a disfunção e morte celular com consequente progressão da DA.pt_BR
dc.publisher.countryBrasilpt_BR
dc.publisher.departmentEscola de Ciências Médicas, Farmacêuticas e Biomédicaspt_BR
dc.publisher.initialsPUC Goiáspt_BR
dc.subject.cnpqCNPQ::CIENCIAS DA SAUDE::MEDICINA::CLINICA MEDICA::NEUROLOGIApt_BR
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dc.degree.graduationMedicina-
dc.degree.levelGraduação-
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