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Keywords:

  • Alzheimer's disease;
  • amyloid beta peptide;
  • preclinical Alzheimer's disease;
  • zinc;
  • zinc transporter proteins;
  • mild clinical impairment

Abstract

Alzheimer's disease (AD), one of the major causes of disability and mortality in Western societies, is a progressive age-related neurodegenerative disorder. Increasing evidence suggests that the etiology of AD may involve disruptions of zinc (Zn) homeostasis. This review discusses current evidence supporting a potential role of Zn and zinc transporters (ZnTs) in processing of the amyloid beta protein precursor (APP) and amyloid beta (Aβ) peptide generation and aggregation.