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Low-copper diet as a preventive strategy for Alzheimer's disease.

Abstract

Copper is an essential element, and either a copper deficiency or excess can be life threatening. Recent studies have indicated that alteration of copper metabolism is one of the pathogenetic mechanisms of Alzheimer's disease (AD). In light of these findings, many researchers have proposed preventive strategies to reduce AD risk. Because the general population comes in contact with copper mainly through dietary intake, that is, food 75% and drinking water 25%, a low-copper diet can reduce the risk of AD in individuals with an altered copper metabolism. We suggest that a diet-gene interplay is at the basis of the "copper phenotype" of sporadic AD. Herein, we describe the pathways regulating copper homeostasis, the adverse sequelae related to its derangements, the pathogenic mechanism of the AD copper phenotype, indications for a low-copper diet, and future perspectives to improve this preventive strategy.

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  • Authors+Show Affiliations

    ,

    Fatebenefratelli Foundation for Health Research and Education, AFaR Division, "San Giovanni Calibita" Fatebenefratelli Hospital, Rome, Italy; Laboratorio di Neurodegenerazione, IRCCS San Raffaele Pisana, Rome, Italy. Electronic address: rosanna.squitti@afar.it.

    ,

    Don Carlo Gnocchi Foundation ONLUS, Milan, Italy.

    Department of Biology, University of Rome "Tor Vergata", Rome, Italy.

    Source

    Neurobiology of aging 35 Suppl 2: 2014 Sep pg S40-50

    MeSH

    Alzheimer Disease
    Cation Transport Proteins
    Ceruloplasmin
    Copper
    Diet
    Drinking Water
    Duodenum
    Female
    Food Analysis
    Genetic Predisposition to Disease
    Hepatolenticular Degeneration
    Homeostasis
    Humans
    Liver
    Male
    Risk

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't
    Review

    Language

    eng

    PubMed ID

    24913894

    Citation

    TY - JOUR T1 - Low-copper diet as a preventive strategy for Alzheimer's disease. AU - Squitti,Rosanna, AU - Siotto,Mariacristina, AU - Polimanti,Renato, Y1 - 2014/05/15/ PY - 2013/11/4/received PY - 2014/2/27/revised PY - 2014/2/27/accepted PY - 2014/5/15/aheadofprint PY - 2014/6/11/entrez PY - 2014/6/11/pubmed PY - 2015/1/21/medline KW - Alzheimer's disease KW - Copper KW - Diet KW - Diet-gene interaction KW - Drinking water KW - Food KW - Genetics KW - Metabolism KW - Prevention KW - Susceptibility SP - S40 EP - 50 JF - Neurobiology of aging JO - Neurobiol. Aging VL - 35 Suppl 2 N2 - Copper is an essential element, and either a copper deficiency or excess can be life threatening. Recent studies have indicated that alteration of copper metabolism is one of the pathogenetic mechanisms of Alzheimer's disease (AD). In light of these findings, many researchers have proposed preventive strategies to reduce AD risk. Because the general population comes in contact with copper mainly through dietary intake, that is, food 75% and drinking water 25%, a low-copper diet can reduce the risk of AD in individuals with an altered copper metabolism. We suggest that a diet-gene interplay is at the basis of the "copper phenotype" of sporadic AD. Herein, we describe the pathways regulating copper homeostasis, the adverse sequelae related to its derangements, the pathogenic mechanism of the AD copper phenotype, indications for a low-copper diet, and future perspectives to improve this preventive strategy. SN - 1558-1497 UR - https://www.unboundmedicine.com/medline/citation/24913894/full_citation L2 - http://linkinghub.elsevier.com/retrieve/pii/S0197-4580(14)00359-5 ER -