A potential role for zinc alterations in the pathogenesis of Alzheimer's disease

Ganna Lyubartseva, Mark A. Lovell

Research output: Contribution to journalReview articlepeer-review

29 Scopus citations

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.

Original languageEnglish
Pages (from-to)98-106
Number of pages9
JournalBioFactors
Volume38
Issue number2
DOIs
StatePublished - Mar 2012

Funding

FundersFunder number
National Institute on AgingP30AG028383

    Keywords

    • Alzheimer's disease
    • Amyloid beta peptide
    • Mild clinical impairment
    • Preclinical Alzheimer's disease
    • Zinc
    • Zinc transporter proteins

    ASJC Scopus subject areas

    • Biochemistry
    • Molecular Medicine
    • Clinical Biochemistry

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