Article

Elevation of zinc transporter ZnT3 protein in the cerebellar cortex of the AbetaPP/PS1 transgenic mouse.

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, PR China.
Journal of Alzheimer's disease: JAD (impact factor: 3.74). 02/2010; 20(1):323-31. DOI:10.3233/JAD-2010-1363 pp.323-31
Source: PubMed

ABSTRACT The presence of senile plaques containing abundant amyloid-beta (Abeta) 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 Abeta 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-beta protein precursor (AbetaPP)/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 Abeta aggregation in the cerebellum of the AbetaPP/PS1 mouse.

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Keywords

Abeta
 
Abeta aggregation
 
AbetaPP)/presenilin 1
 
AbetaPP/PS1 mouse
 
abundant amyloid-beta
 
AD brains
 
amyloid plaques
 
amyloid-beta protein precursor
 
Confocal microscopic
 
elevated expression
 
immunoblotting assay
 
major pathological hallmarks
 
overexpression
 
peripheral parts
 
plaques
 
rosette-shaped plaques
 
senile plaques
 
zinc metabolic disturbances
 
ZnT3 immunofluorescence
 
ZnT3 protein