Affiliations: [a] Key Laboratory of Cell Biology of Ministry of Public Health of China, Laboratory of Cell Engineering and Therapy of Institute of Tissue Engineering, China Medical University, Shenyang, P.R. China | [b] The First Clinical Hospital, China Medical University, Shenyang, P.R. China | [c] Institute of Anatomy, University of Aarhus, Aarhus C, Denmark
Correspondence:
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Correspondence to: Zhan-You Wang, Key Laboratory of Cell Biology of Ministry of Public Health of China, Laboratory of Cell Engineering and Therapy of Institute of Tissue Engineering, China Medical University, Shenyang 110001, P.R. China. Tel.: +86 24 23256666 5305; Fax: +86 24 23256666 5305; E-mail: [email protected].
Note: [] Handling Associate Editor: Ashley Bush
Abstract: The presence of senile plaques containing abundant amyloid-β (Aβ) peptide is one of the major pathological hallmarks of Alzheimer's disease (AD). Recent studies support the notion that overexpression of zinc transporters (ZnT) is involved in zinc metabolic disturbances and Aβ aggregation in AD brains. Here we present data showing an elevated expression of zinc transporter 3 (ZnT3) protein, revealed by immunoblotting assay, in the cerebellum of the amyloid-β protein precursor (AβPP)/presenilin 1 (PS1) transgenic mouse. Confocal microscopic and autometallographic results showed that ZnT3 immunofluorescence and zinc ions were predominantly located in the amyloid plaques. ZnT3 protein was abundantly distributed throughout the plaques, whereas zinc ions were mainly located in the peripheral parts of rosette-shaped plaques with a lightly stained center. Collectively, our results suggest that ZnT3 protein is involved in the Aβ aggregation in the cerebellum of the AβPP/PS1 mouse.
