Journal
BRAIN RESEARCH BULLETIN
Volume 77, Issue 1, Pages 55-60Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.brainresbull.2008.03.014
Keywords
autometallography; beta-amyloid peptide; human brain; immunofluorescence; senile plaque
Categories
Funding
- Natural Science Foundation of China [30670722, 30770680]
- Program for New Century Excellent Talents in University [NCET-04-0288]
- China Postdoctoral Science Foundation [2005037008]
- Specialized Research Fund for the Doctoral Program of Higher Education [SRFDP-20060159001]
- United States Department of Agriculture [CRIS-5603-515-30-014-OOD]
- Augustinus Foundation
- Aarhus University Research Foundation
- Aase & Ejnar Danielsens Fund
- Danish Medical Association Research Fund
- Beckett Foundation
- Lundbeck Foundation of Denmark
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The pathological key features of Alzheimer's disease (AD) are beta-amyloid peptide (A beta)-containing senile plaques (SP) and neurofibrillary tangles. Previous studies have suggested that an extracellular elevation of the zinc concentration can initiate the deposition of A beta and lead to the formation of SP. In the present study, we present data showing a correlation between zinc ions, zinc transporters (ZNTs) and AD, using immersion auto metallography (AMG) and double immunofluorescence for the ZNTs and A beta. We found that all the ZNTs tested (ZNT1, 3,4,5,6, 7) were extensively present in the A beta-positive plaques in the cortex of human AD brains, and the density of autometallographic silver enhanced zinc-sulphur nanoparticles were much higher in the plaques than in the surrounding zinc enriched (ZEN) terminals. Moreover, we found an abundant expression of ZNT3 and autometallographic grains in the amyloid angiopathic vessels. The subcellular localization of ZNTs and zinc ions were not detected, due to the limited tissue preservation in the present study. In conclusion, our data provided significant morphological evidence of zinc ions and ZNTs being actively involved in the pathological processes that lead to plaque formation. (c) 2008 Elsevier Inc. All rights reserved.
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