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

J Alzheimers Dis. 2010;20(1):323-31. doi: 10.3233/JAD-2010-1363.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / genetics
  • Alzheimer Disease / pathology*
  • Amyloid beta-Protein Precursor / genetics
  • Amyloid beta-Protein Precursor / metabolism
  • Animals
  • Cation Transport Proteins / metabolism*
  • Cerebellar Cortex / metabolism*
  • Cerebellar Cortex / pathology
  • Disease Models, Animal
  • Gene Expression Regulation / genetics*
  • Humans
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Microscopy, Confocal / methods
  • Mutation
  • Presenilin-1 / genetics
  • Presenilin-1 / metabolism
  • Zinc / metabolism

Substances

  • Amyloid beta-Protein Precursor
  • Cation Transport Proteins
  • PSEN1 protein, human
  • Presenilin-1
  • SLC30A3 protein, human
  • Zinc