MICROGLIAL PHAGOCYTOSIS IN RATS WITH DIFFERENT MODELS OF ALZHEIMER'S DISEASE

Neuroinflammation is a key feature of Alzheimer's disease (AD), progressive neurodegenerative disorder. Microglia, the resident immune cells central nervous system, play crucial role in pathogenesis AD and are active participants neuroinflammation. Adequate reproduction neuroinflammation animal models one main methodological approaches for studying pathophysiology. The aim study was to conduct comparative assessment phagocytic activity microglia rats with induced by intrahippocampal administration beta-amyloid (Aβ) 1-40 Aβ25-35. Materials methods. Wistar male were used study. Intact sham-operated animals as controls. development confirmed cognitive impairment Barnes maze behavioral test, well level dopaminergic neurons (DN). microglia, oxidative metabolism expression phenotypic markers CD80 CD206 determined flow cytometry. Results. In Aβ 1-40-induced AD, significant loss DN registered, microglial characterized an increase proportion their endocytic activity, augmented overexpression CD86 CD206. 25-35-induced moderate observed, only number phagocytizing without changes metabolism, markers. Conclusion. Thus, Aβ1–40-induced pro-inflammatory functional profile which characteristic clinical course disease, more adequately reproduced.