Fig. 8
From: Amelioration of amyloid-β-induced deficits by DcR3 in an Alzheimer’s disease model
Working model: In the presence of Aβ, microglia polarize toward the M1 phenotype and secrete pro-inflammatory cytokines, which trigger neurodegeneration. DcR3 interacts with HSPGs and drives microglia polarization to the IL-4+YM1+ M2a-like subtype that secrete more anti-inflammatory cytokines. This change enhances Aβ phagocytosis, thereby reducing amyloid plaques and cognitive deficits in APP mice