Neuroinflamação na doença de Alzheimer: uma revisão da literatura

Abstract

Alzheimer'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.