The abnormal accumulation of amyloid-β oligomers (oAβ 42) and protofibrils within neuronal/microglial cells is believed to be crucial to Alzheimer’s disease (AD) progression. As a result, the inflammation induced by pro-inflammatory cytokines was greatly alleviated. The phagocytic uptake of mpAβ 42 by microglia was enhanced significantly as compared to the counterpart of oAβ 42, and the M1 polarization of microglia often occurring after the uptake of oAβ 42 restricted to an appreciable extent. In addition to the good preservation of neurite outgrowth through the diminished uptake of oAβ 42, neurons treated with oAβ 42 under magnetic stirring also exhibited comparable neuron-specific protein expression to those in the absence of oAβ 42. With oAβ 42 being effectively converted into mpAβ 42, the neurotoxicity toward neuronal cells was thus greatly reduced. In this work, a novel strategy adopting silica-coated iron oxide stir bar (MSB)-based AD therapy system via magnetic stirring-induced capture of oAβ 42 into magnetic plaques (mpAβ 42) and activation of microglia on cellular plaque clearance was developed. Soluble amyloid-β oligomers (oAβ 42)-induced neuronal death and inflammation response has been recognized as one of the major causes of Alzheimer’s disease (AD).
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