Disruption of zinc homeostasis in Alzheimer's disease

J. D. Robertson, A. M. Crafford, W. R. Markesbery, M. A. Lovell

Research output: Contribution to journalArticlepeer-review

12 Scopus citations


The basic hypothesis being tested is that, in Alzheimer's disease (AD), the delicate balance of brain Zn is disrupted and may play a role in the pathogenesis of neuron degeneration. Micro-PIXE measurements reveal a significant elevation of Zn in senile plaques (SP) in AD brain compared with adjacent neuropil and a significant increase in AD neuropil compared to control neuropil. The observation of elevated Zn in SP is of interest because the amyloid precursor protein contains a Zn binding site that may prevent normal cleavage leading to the generation of a toxic fragment of beta amyloid, the constituent of SP. The potential of using laser-ablation inductively coupled plasma mass spectrometry as a complimentary microprobe technique is also presented.

Original languageEnglish
Pages (from-to)454-458
Number of pages5
JournalNuclear Instruments and Methods in Physics Research, Section B: Beam Interactions with Materials and Atoms
Issue number1-4
StatePublished - Apr 2002

Bibliographical note

Funding Information:
Funding for this work was provided by NIH Grants 5-P01-AG05119, 5-P50-AG05144 and 1R01-AG16269 and by a grant from the Abercrobmie Foundation. The authors thank Ela Patel for tissue immunostaining and Barry Higgins for assistance with the LA-ICP-MS measurements.


  • Alzheimer's disease
  • Brain
  • Micro-PIXE
  • Zinc

ASJC Scopus subject areas

  • Nuclear and High Energy Physics
  • Instrumentation


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