Astrócitos e disfunção cognitiva: papel na modulação neural e consequências da senescência
DOI:
https://doi.org/10.34119/bjhrv9n2-050Keywords:
Doença de Alzheimer, astrócitos, micróglia, neuroinflamação, sinapse tripartiteAbstract
Considerando que a Doença de Alzheimer (DA) representa a principal causa de demência no mundo e que sua fisiopatologia clássica, baseada na deposição de beta-amiloide (Aβ) e proteína tau hiperfosforilada, não explica integralmente a progressão do declínio cognitivo, torna-se necessário investigar mecanismos celulares adicionais envolvidos na neurodegeneração. Objetiva-se analisar as evidências científicas que correlacionam a disfunção das células da glia — especialmente astrócitos e micróglia — com a progressão da DA. Para tanto, procede-se a uma revisão integrativa da literatura, com busca nas bases PubMed e LILACS, utilizando descritores relacionados à Doença de Alzheimer, astrócitos, micróglia, sinapse tripartite e neurodegeneração, incluindo estudos publicados entre 2015 e 2025. Desse modo, observa-se que a ativação glial crônica induzida pelo acúmulo de Aβ e pelo estresse oxidativo promove a liberação de citocinas pró-inflamatórias, espécies reativas de oxigênio e óxido nítrico, favorecendo disfunção mitocondrial, perda sináptica e apoptose neuronal. A senescência astrocitária, associada ao fenótipo secretor inflamatório (SASP), intensifica esse processo. Conclui-se que a disfunção integrada de astrócitos e micróglia estabelece um ciclo persistente de neuroinflamação que impulsiona o declínio cognitivo na DA.
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