Altered expression of zinc transporters-4 and -6 in mild cognitive impairment, early and late Alzheimer's disease brain

J. L. Smith, S. Xiong, W. R. Markesbery, M. A. Lovell

Research output: Contribution to journalArticlepeer-review

88 Scopus citations


Accumulating evidence suggests that a disruption of zinc (Zn) homeostasis may play a role in the pathogenesis of Alzheimer's disease. Although several Zn transporter proteins responsible for the regulation of Zn balance are present in the brain, there has been little study of these proteins in Alzheimer's disease. To determine if alterations of Zn transporter proteins exist, levels of Zn transporter-4, which functions to remove Zn from the cytoplasm to endosomal/lysosomal compartments, and Zn transporter-6, which allocates cytoplasmic Zn to the trans-Golgi network, were measured in the hippocampus/parahippocampal gyrus, superior and middle temporal gyrus, and cerebellum of subjects with mild cognitive impairment, early Alzheimer's disease, late stage Alzheimer's disease, and age-matched controls using Western blot analysis and protein specific antibodies. Our results show that Zn transporter-4 and Zn transporter-6 are significantly (P<0.05) increased in hippocampus/parahippocampal gyrus of early Alzheimer's disease and Alzheimer's disease subjects. Zn transporter-6 is also increased (P<0.1) in the superior and middle temporal gyrus of Alzheimer's disease brain.

Original languageEnglish
Pages (from-to)879-888
Number of pages10
Issue number3
StatePublished - 2006

Bibliographical note

Funding Information:
The authors thank Paula Thomason for editorial assistance and Sonya Anderson for subject demographic data. This work was supported by National Institutes of Health grants 1-RO1-AG16269, 5P50-AG05144 and 5P01-AG05119 and by a grant from the Abercrombie Foundation.


  • AD
  • Alzheimer's disease
  • MCI
  • ZnT
  • mild cognitive impairment
  • zinc transporters

ASJC Scopus subject areas

  • General Neuroscience


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