Abstract

Neuroinflammation has emerged as a key player in the pathogenesis of Alzheimer's disease (AD), contributing to the progression and severity of cognitive decline. In AD, the brain's immune response, mediated by microglia and astrocytes, becomes dysregulated, resulting in chronic neuroinflammation that accelerates neuronal damage. This review explores the mechanisms underlying neuroinflammation in AD, focusing on the activation of glial cells, the release of pro-inflammatory cytokines, and the subsequent neurodegeneration. Additionally, we examine potential biomarkers of neuroinflammation that could aid in early diagnosis and prognosis, such as elevated levels of C-reactive protein (CRP) and pro-inflammatory cytokines. The therapeutic implications of targeting neuroinflammatory pathways are also discussed, with a particular focus on the development of anti-inflammatory drugs that could slow or halt disease progression. Despite promising results in preclinical studies, translating these findings into clinical practice remains challenging. This review highlights the need for further research to identify effective therapies that specifically target neuroinflammation in AD.