Modulação microglial na doença de Alzheimer

• Autor(a) principal: Barbosa, Marina Zanichelli [UNESP]
• Data de Publicação: 2016
• Tipo de documento: Trabalho de conclusão de curso
• Idioma: por
• Título da fonte: Repositório Institucional da UNESP
• Texto Completo: http://hdl.handle.net/11449/203852; http://www.athena.biblioteca.unesp.br/exlibris/bd/capelo/2019-01-28/000897937.pdf
• topic: Alzheimer, Doença de; Cerebro - Doenças; Microglia; Camundongo como animal de laboratorio; Brain - Diseases

There are many questions to be solved about Alzheimer's Disease (AD), although studies are advancing significantly. There are many unenlightened mechanisms about pathogenesis and no form of prevention or cure. It is known that in the development of the disease the microglia can undergo alteration of phenotype and that this can directly influence the neuron. In order to understand more about the neuroimmune interactions existing in Alzheimer's disease, this project has as main objective to investigate when and how the M2 microglia pattern changes to M1 in the triple transgenic model (3xTg-AD), the murine model that most closely resembles the disease in humans. This pattern change reflects on neurodegeneration and is related to beta-amyloid plaques and neurofibrillary tangles. We know that increased production of reactive oxygen species (ROS) accompanies the change from M2 to M1 phenotype, which is responsible for the release of proinflammatory cytokines that may be directly toxic to neurons. Therefore, we want to know at what moment and what mechanism is involved in the change of the microglia activation pathway from the alternative phenotype (M2) to the classic (M1) in 3xTg-AD mice, the AD triple transgenic model.