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Capturing Amyloid-β Oligomers by Stirring with Microscaled Iron Oxide Stir Bars into Magnetic Plaques to Reduce Cytotoxicity toward Neuronal Cells.


ABSTRACT: Soluble amyloid-β oligomers (oAβ42)-induced neuronal death and inflammation response has been recognized as one of the major causes of Alzheimer's disease (AD). In this work, a novel strategy adopting silica-coated iron oxide stir bar (MSB)-based AD therapy system via magnetic stirring-induced capture of oAβ42 into magnetic plaques (mpAβ42) and activation of microglia on cellular plaque clearance was developed. With oAβ42 being effectively converted into mpAβ42, the neurotoxicity toward neuronal cells was thus greatly reduced. In addition to the good preservation of neurite outgrowth through the diminished uptake of oAβ42, neurons treated with oAβ42 under magnetic stirring also exhibited comparable neuron-specific protein expression to those in the absence of oAβ42. The phagocytic uptake of mpAβ42 by microglia was enhanced significantly as compared to the counterpart of oAβ42, and the M1 polarization of microglia often occurring after the uptake of oAβ42 restricted to an appreciable extent. As a result, the inflammation induced by pro-inflammatory cytokines was greatly alleviated.

SUBMITTER: Tsai YC 

PROVIDER: S-EPMC7407479 | biostudies-literature | 2020 Jun

REPOSITORIES: biostudies-literature

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Capturing Amyloid-β Oligomers by Stirring with Microscaled Iron Oxide Stir Bars into Magnetic Plaques to Reduce Cytotoxicity toward Neuronal Cells.

Tsai Yuan-Chung YC   Luo Jing-Chian JC   Liu Te-I TI   Lu I-Lin IL   Shen Ming-Yin MY   Chuang Chun-Yu CY   Chern Chorng-Shyan CS   Chiu Hsin-Cheng HC  

Nanomaterials (Basel, Switzerland) 20200630 7


Soluble amyloid-β oligomers (oAβ<sub>42</sub>)-induced neuronal death and inflammation response has been recognized as one of the major causes of Alzheimer's disease (AD). 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<sub>42</sub> into magnetic plaques (mpAβ<sub>42</sub>) and activation of microglia on cellular plaque clearance was developed. With oAβ<sub>42</sub> being effectively converted in  ...[more]

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