Abstract
Objective: To analyze the role of neuroinflammation in dementia, aiming to identify therapeutic targets for treatment and prevention. Bibliographic review: Neuroinflammation is central to the progression of dementias, such as Alzheimer's disease (AD) and cognitive vascular dementia (VCID), mediated by the activation of glial cells that release pro-inflammatory and neurotoxic cytokines, promoting neurodegeneration. Investigation of glial cells reveals their crucial role in the immune response and maintenance of brain homeostasis, highlighting the importance of balancing pro- and anti-inflammatory cytokines in modulating neuroinflammation. Advances in diagnosis and treatment, including biomarkers such as translocator protein (TSPO) and targeted therapeutic strategies, show promise in mitigating the effects of neuroinflammation. Final considerations: Neuroinflammation is crucial in the progression of dementia, acting synergistically with other pathological mechanisms and accelerating neurodegeneration. Evidence points to the modulation of inflammation as a promising therapeutic strategy. However, complexity requires personalized approaches, with an emphasis on identifying specific biomarkers and phenotypes. Future research focused on these areas may offer new directions for more effective interventions, transforming dementia management.
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