NEUROINFLAMMATION AS A KEY MECHANISM IN THE PROGRESSION OF ALZHEIMER'S: NEW THERAPEUTIC PERSPECTIVES

• DOI: https://doi.org/10.22533/at.ed.15951625240311

• Palavras-chave: Cytokines; Alzheimer's Disease; Microglia; Neuroinflammation; Anti-inflammatory Therapies.

• Keywords: Cytokines; Alzheimer's Disease; Microglia; Neuroinflammation; Anti-inflammatory Therapies.

• Abstract:

  INTRODUCTION: Alzheimer's disease (AD) is a progressive neurodegenerative condition that causes cognitive decline, memory loss and functional impairment, affecting millions of people worldwide. Neuroinflammation, caused by excessive activation of glial cells such as microglia and astrocytes, has been identified as a central factor in the progression of the disease, exacerbating neuronal degeneration and synaptic dysfunction. OBJECTIVE: To analyze neuroinflammation as a key mechanism in the progression of AD, in addition to exploring new therapeutic perspectives that can modulate the cerebral inflammatory response, such as the use of inflammatory cytokine inhibitors and microglia modulators. METHODOLOGY: The methodology adopted was a systematic literature review, with the search and analysis of articles published between 2020 and 2024, in the main scientific databases. The search was carried out in the VHL, LILACS, MEDLINE and SCIELO databases, using specific descriptors such as "Neuroinflammation", "Alzheimer's Disease", "Microglia", "Cytokines" and "Anti-inflammatory Therapies". After applying strict inclusion and exclusion criteria, 18 articles were selected that addressed the role of neuroinflammation in AD and its therapeutic implications. Analysis of these studies provided a solid basis on emerging therapeutic approaches to modulating neuroinflammation in AD. RESULTS AND DISCUSSION: Neuroinflammation plays a central role in the progression of Alzheimer's disease (AD), accelerating neurodegeneration and cognitive impairment. Chronic activation of microglia and astrocytes generates inflammatory mediators that aggravate oxidative stress, compromise neuronal function and affect synaptic plasticity, which is essential for memory. In addition, neuroinflammation impairs the removal of toxic proteins such as beta-amyloid, favoring the accumulation of amyloid plaques. Neuroinflammation starts early, before the clinical symptoms of AD, and intervening in it could slow down the progression of the disease. Chronic inflammation affects mitochondrial function and the formation of new synaptic connections, which are essential for cognition. CONCLUSION: Controlling neuroinflammation and restoring affected cellular processes could be an effective therapeutic strategy for slowing the progression of AD. Therapies such as inflammatory cytokine inhibitors and microglia modulators show promising results, although more clinical studies are needed.