Abstract
<jats:p>Alzheimer’s disease (AD) is one of the most common causes of cognitive impairment in the elderly, the pathogenesis of which involves the accumulation of amyloid plaques, hyperphosphorylation of Tau protein, and neuroinflammation. In recent years, special attention has been paid to the role of microglia and monocytes in the development and progression of AD. Microglia, as an innate immune cell of the central nervous system, participates in the phagocytosis of amyloid plaques, protection of neurons, and maintenance of homeostasis. However, its prolonged activation leads to the predominance of a pro-inflammatory phenotype and the deepening of neuronal degeneration. At the same time, monocytes can be recruited to the brain tissue and contribute to the clearance of Aβ, acting as an additional source of microglia. Thus, it becomes clear that activities involving the activation/modulation of microglia and monocytes show promise for the treatment of AR. The presented work summarizes current data on the interaction between microglia and monocytes, phenotypic plasticity, and their impact on the pathogenesis of AD, highlighting the possibilities of therapeutic targeting of these cells.</jats:p>