Folate Deficiency Increased Microglial Amyloid-β Phagocytosis via the RAGE Receptor in Chronic Unpredictable Mild-Stress Rat and BV2 Cells

Depression is often considered one of the prevalent neuropsychiatric symptoms Alzheimer’s disease (AD). β-amyloid (Aβ) metabolism disorders and impaired microglia phagocytosis are potential pathological mechanisms between depression AD. Folate deficiency (FD) a risk factor for In this study, we used chronic unpredictable mild stress (CUMS) rat model Aβ by BV2 cells to explore which FD affects The results revealed that exacerbated depressive behavior activated in CUMS rats, leading an increase intracellular phagocytosis-related receptors advanced glycation end products (RAGE). Then, vitro showed expression RAGE receptor M2 phenotype marker (CD206) were upregulated treatment cells, phagocytosis. However, there was no significant difference toll-like 4 (TLR4) clathrin heavy chain (CHC). Furthermore, when using RAGE-specific inhibitor FPS-ZM1, uptake folate-normal (FN) cell groups. conclusion, these findings suggest may promote via regulating or under treatment.