Alzheimer's Disease (AD), the most prevalent neurodegenerative disorder, is the leading cause of dementia in older adults and is closely associated with chronic neuroinflammation within the central nervous system. The hallmark pathological features of AD include neurofibrillary tangles, amyloid -β plaques, and extensive neuronal loss. Although amyloid-β has been extensively studied, the development of effective disease-modifying therapies remains limited in clinical practice. Novel therapeutic approaches are increasingly focused on modulating these immune mechanisms, such as altering microglial phenotypes, inhibiting the NLRP3 inflammasome, regulating NF-κB and JAK/STAT signalling, and employing cytokine-based interventions. Additionally, stem cell-derived therapies and extracellular vesicles with strong immunomodulatory properties have emerged as promising candidates. This review aims to deepen the understanding of immunoregulatory and inflammatory mechanisms in Alzheimer's disease and to support the development of novel antiinflammatory therapies that may slow or prevent disease progression.
Katiyar et al. (2026) studied this question.