View Item 

Show simple item record

Copper excess, zinc deficiency, and cognition loss in Alzheimer's disease
dc.contributor.authorCristina Polidori, Mariaen_US
dc.date.accessioned2012-04-04T18:42:07Z
dc.date.available2013-05-01T17:24:43Zen_US
dc.date.issued2012-03en_US
dc.identifier.citationCristina Polidori, Maria (2012). "Copper excess, zinc deficiency, and cognition loss in Alzheimer's disease." BioFactors 38(2): 107-113. <http://hdl.handle.net/2027.42/90519>en_US
dc.identifier.issn0951-6433en_US
dc.identifier.issn1872-8081en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/90519
dc.description.abstractIn this special issue about biofactors causing cognitive impairment, we present evidence for and discuss two such biofactors. One is excess copper, causing neuronal toxicity. The other is zinc deficiency, causing neuronal damage. We present evidence that Alzheimer's disease (AD) has become an epidemic in developed, but not undeveloped, countries and that the epidemic is a new disease phenomenon, beginning in the early 1900s and exploding in the last 50 years. This leads to the conclusion that something in the developed environment is a major risk factor for AD. We hypothesize that the factor is inorganic copper, leached from the copper plumbing, the use of which coincides with the AD epidemic. We present a web of evidence supporting this hypothesis. Regarding zinc, we have shown that patients with AD are zinc deficient when compared with age‐matched controls. Zinc has critical functions in the brain, and lack of zinc can cause neuronal death. A nonblinded study about 20 years ago showed considerable improvement in AD with zinc therapy, and a mouse AD model study also showed significant cognitive benefit from zinc supplementation. In a small blinded study we carried out, post hoc analysis revealed that 6 months of zinc therapy resulted in significant benefit relative to placebo controls in two cognitive measuring systems. These two factors may be linked in that zinc therapy significantly reduced free copper levels. Thus, zinc may act by lowering copper toxicity or by direct benefit on neuronal health, or both.en_US
dc.publisherWiley Subscription Services, Inc., A Wiley Companyen_US
dc.subject.otherZincen_US
dc.subject.otherCognitionen_US
dc.subject.otherAlzheimer's Diseaseen_US
dc.subject.otherCopperen_US
dc.titleCopper excess, zinc deficiency, and cognition loss in Alzheimer's diseaseen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelMolecular, Cellular and Developmental Biologyen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartment of Human Genetics, Medical School University of Michigan, Ann Arbor 48103, MI, USAen_US
dc.contributor.affiliationumDepartment of Human Genetics, Medical School University of Michigan, Ann Arbor, MI, USAen_US
dc.contributor.affiliationotherAdeona Pharmaceuticals, Ann Arbor, MI, USAen_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/90519/1/1005_ftp.pdf
dc.identifier.doi10.1002/biof.1005en_US
dc.identifier.sourceBioFactorsen_US
dc.identifier.citedreferenceMorris, M. C., Evans, D. A., Tangney, C. C., Bienias, J. L., Schneider, J. A., Wilson, R. S., and Scherr, P. A. ( 2006 ) Dietary copper and high saturated and trans fat intakes associated with cognitive decline. Arch. Neurol. 63, 1085 – 1088.en_US
dc.identifier.citedreferenceSparks, D. L. and Schreurs, B. G. ( 2003 ) Trace amounts of copper in water induce β‐amyloid plaques and learning deficits in a rabbit model of Alzheimer's disease. Proc. Natl. Acad. Sci. USA 100, 11065 – 11069.en_US
dc.identifier.citedreferenceSparks, D. L., Friedland, R., Petanceska, S., Schreurs, B. G., Shi, J., Perry, G., Smith, M. A., Sharma, A., Derosa, S., Ziolkowski, C., and Stankovic, G. ( 2006 ) Trace copper levels in the drinking water, but not zinc or aluminum, influence CNS Alzheimer‐like pathology. J. Nutr. Health Aging 10, 247 – 254.en_US
dc.identifier.citedreferenceDeane, R., Sagare, A., Coma, M., Parisi, M., Gelein, R., Singh, I., and Zlokovic, B. ( 2007 ) Paper Presentation at the Annual Meeting of the Society for Neuroscience, San Diego, CA.en_US
dc.identifier.citedreferenceSquitti, R., Pasqualetti, P., Dal Forno, G., Moffa, F., Cassetta, E., Lupoi, D., Vernieri, F., Rossi, L., Baldassini, M., and Rossini, P. M. ( 2005 ) Excess of serum copper not related to ceruloplasmin in Alzheimer disease. Neurology 64, 1040 – 1046.en_US
dc.identifier.citedreferenceBrewer, G. J., Dick, R. D., Johnson, V. D., Brunberg, J. A., Kluin, K. J., and Fink, J. K. ( 1998 ) Treatment of Wilson's disease with zinc: XV long‐term follow‐up studies. J. Lab. Clin. Med. 132, 264 – 278.en_US
dc.identifier.citedreferenceSquitti, R., Barbati, G., Rossi, L., Ventriglia, M., Dal Forno, G., Cesaretti, S., Moffa, F., Caridi, I., Cassetta, E., Pasqualetti, P., Calabrese, L., Lupoi, D., and Rossini, P. M. ( 2006 ) Excess of nonceruloplasmin serum copper in AD correlates with MMSE, CSF [β]‐amyloid, and h‐tau. Neurology 67, 76 – 82.en_US
dc.identifier.citedreferenceSquitti, R., Bressi, F., Pasqualetti, P., Bonomini, C., Ghidoni, R., Binetti, G., Cassetta, E., Moffa, F., Ventriglia, M., Vernieri, F., and Rossini, P. M. ( 2009 ) Longitudinal prognostic value of serum “free” copper in patients with Alzheimer disease. Neurology 72, 50 – 55.en_US
dc.identifier.citedreferenceSalustri, C., Barbati, G., Ghidoni, R., Quintiliani, L., Ciappina, S., Binetti, G., and Squitti, R. ( 2010 ) Is cognitive function linked to serum free copper levels? A cohort study in a normal population. Clin. Neurophysiol. 121, 502 – 507.en_US
dc.identifier.citedreferenceNose, Y., Kim, B. E., and Thiele, D. J. ( 2006 ) Ctr1 drives intestinal copper absorption and is essential for growth, iron metabolism, and neonatal cardiac function. Cell Metab. 4, 235 – 244.en_US
dc.identifier.citedreferenceHill, G. M., Brewer, G. J., Juni, J. E., Prasad, A. S., and Dick, R. D. ( 1986 ) Treatment of Wilson's disease with zinc. II. Validation of oral 64copper with copper balance. Am. J. Med. Sci. 292, 344 – 349.en_US
dc.identifier.citedreferenceBrewer, G. J., Kanzer, S. H., Zimmerman, E. A., Molho, E. S., Celmins, D. F., Heckman, S. M., and Dick, R. ( 2010 ) Subclinical zinc deficiency in Alzheimer's disease and Parkinson's disease. Am. J. Alzheimers Dis. Other Demen. 25, 572 – 575.en_US
dc.identifier.citedreferenceBaum, L., Chan, I. H., Cheung, S. K., Goggins, W. B., Mok, V., Lam, L., Leung, V., Hui, E., Ng, C., Woo, J., Chiu, H. F., Zee, B. C., Cheng, W., Chan, M. H., Szeto, S., Lui, V., Tsoh, J., Bush, A. I., Lam, C. W., and Kwok, T. ( 2010 ) Serum zinc is decreased in Alzheimer's disease and serum arsenic correlates positively with cognitive ability. Biometals 23, 173 – 179.en_US
dc.identifier.citedreferenceAdlard, P. A., Parncutt, J. M., Finkelstein, D. I., and Bush, A. I. ( 2010 ) Cognitive loss in zinc transporter‐3 knock‐out mice: a phenocopy for the synaptic and memory deficits of Alzheimer's disease?. J. Neurosci. 30, 1631 – 1636.en_US
dc.identifier.citedreferenceTakeda, A. ( 2010 ) Insight into glutamate excitotoxicity from synaptic zinc homeostasis. Int. J. Alzheimers Dis. 2011, 491597.en_US
dc.identifier.citedreferenceCrouch, P. J., Savva, M. S., Hung, L. W., Donnelly, P. S., Mot, A. I., Parker, S. J., Greenough, M. A., Volitakis, I., Adlard, P. A., Cherny, R. A., Masters, C. L., Bush, A. I., Barnham, K. J., and White, A. R. ( 2011 ) The Alzheimer's therapeutic PBT2 promotes amyloid‐β degradation and GSK3 phosphorylation via a metal chaperone activity. J. Neurochem. 119, 220 – 230.en_US
dc.identifier.citedreferenceConstantinidis, J. ( 1992 ) Treatment of Alzheimer's disease by zinc compounds. Drug Dev. Res. 27, 1 – 14.en_US
dc.identifier.citedreferenceCorona, C., Masciopinto, F., Silvestri, E., Viscovo, A. D., Lattanzio, R., Sorda, R. L., Ciavardelli, D., Goglia, F., Piantelli, M., Canzoniero, L. M., and Sensi, S. L. ( 2010 ) Dietary zinc supplementation of 3xTg‐AD mice increases BDNF levels and prevents cognitive deficits as well as mitochondrial dysfunction. Cell Death Dis. 1, e91.en_US
dc.identifier.citedreferenceBrewer, G. J. and Yuzbasiyan‐Gurkan, V. ( 1992 ) Wilson disease. Medicine (Baltimore) 71, 139 – 164.en_US
dc.identifier.citedreferenceBrewer, G. J., Terry, C. A., Aisen, A. M., and Hill, G. M. ( 1987 ) Worsening of neurologic syndrome in patients with Wilson's disease with initial penicillamine therapy. Arch. Neurol. 44, 490 – 493.en_US
dc.identifier.citedreferenceBrewer, G. J., Askari, F., Lorincz, M. T., Carlson, M., Schilsky, M., Kluin, K. J., Hedera, P., Moretti, P., Fink, J. K., Tankanow, R., Dick, R. B., and Sitterly, J. ( 2006 ) Treatment of Wilson disease with ammonium tetrathiomolybdate. IV. Comparison of tetrathiomolybdate and trientine in a double‐blind study of treatment of the neurologic presentation of Wilson disease. Arch. Neurol. 63, 521 – 527.en_US
dc.identifier.citedreferenceAlzheimer, A. ( 1907 ) Ueber einer eigenartige Erkrankung der Hirnrinde. Allg. Z. Psychiatr. 64, 146 – 148.en_US
dc.identifier.citedreferenceAlzheimer's Association ( 2010 ) Alzheimer's Disease Facts and Figures. Alzheimer's Disease Association, Chicago, Illinois. pp. 1 – 74.en_US
dc.identifier.citedreferenceHardy, J. A. and Higgins, G. A. ( 1992 ) Alzheimer's disease: the amyloid cascade hypothesis. Science 256, 184 – 185.en_US
dc.identifier.citedreferenceSayre, L. M., Perry, G., Harris, P. L., Liu, Y., Schubert, K. A., and Smith, M. A. ( 2000 ) In situ oxidative catalysis by neurofibrillary tangles and senile plaques in Alzheimer's disease: a central role for bound transition metals. J. Neurochem. 74, 270 – 279.en_US
dc.identifier.citedreferenceMiyata, M. and Smith, J. D. ( 1996 ) Apolipoprotein E allele‐specific antioxidant activity and effects on cytotoxicity by oxidative insults and β‐amyloid peptides. Nat. Genet. 14, 55 – 61.en_US
dc.identifier.citedreferenceSeshadri, S., Beiser, A., Selhub, J., Jacques, P. F., Rosenberg, I. H., D'Agostino, R. B., Wilson, P. W., and Wolf, P. A. ( 2002 ) Plasma homocysteine as a risk factor for dementia and Alzheimer's disease. N. Engl. J. Med. 346, 476 – 483.en_US
dc.identifier.citedreferenceMoalem, S., Percy, M. E., Andrews, D. F., Kruck, T. P., Wong, S., Dalton, A. J., Mehta, P., Fedor, B., and Warren, A. C. ( 2000 ) Are hereditary hemochromatosis mutations involved in Alzheimer disease? Am. J. Med. Genet. 93, 58 – 66.en_US
dc.identifier.citedreferenceZambenedetti, P., De Bellis, G., Biunno, I., Musicco, M., and Zatta, P. ( 2003 ) Transferrin C2 variant does confer a risk for Alzheimer's disease in caucasians. J. Alzheimers Dis. 5, 423 – 427.en_US
dc.identifier.citedreferenceGrant, W. B. ( 1997 ) Dietary links to Alzheimer's disease. Alzheimers Dis. Rev. 2, 42 – 55.en_US
dc.identifier.citedreferenceOsler, W., ed. ( 1910 ) Modern Medicine in Theory and Practice. Lea and Febiger, Philadelphia, PA.en_US
dc.identifier.citedreferenceGowers, W. R. ( 1888 ) A Manual of Diseases of the Nervous System. P Blakiston, Son, and Co, Philadelphia, PA.en_US
dc.identifier.citedreferenceStrachey, J., Freud, A., Strachey, A., and Tyson, A., eds. ( 1966 ) The Standard Edition of the Complete Psychological Works of Sigmund Freud. The Hogarth Press and the Institute of Psycho‐Analysis, London.en_US
dc.identifier.citedreferenceBoyd, W. ( 1938 ) A Textbook of Pathology: An Introduction to Medicine. Lea and Febiger, Philadelphia, PA.en_US
dc.identifier.citedreferenceWaldman, M. and Lamb, M. ( 2005 ) Dying for a Hamburger: Modern Meat Processing and the Epidemic of Alzheimer's Disease 1st edn. Thomas Dune Books/St. Martin's Press, New York.en_US
dc.identifier.citedreferenceUeda, K., Kawano, H., Hasuo, Y., and Fujishima, M. ( 1992 ) Prevalence and etiology of dementia in a Japanese community. Stroke 23, 798 – 803.en_US
dc.identifier.citedreferenceWhite, L., Petrovitch, H., Ross, G. W., Masaki, K. H., Abbott, R. D., Teng, E. L., Rodriguez, B. L., Blanchette, P. L., Havlik, R. J., Wergowske, G., Chiu, D., Foley, D. J., Murdaugh, C., and Curb, J. D. ( 1996 ) Prevalence of dementia in older Japanese‐American men in Hawaii: the Honolulu‐Asia Aging Study. JAMA 276, 955 – 960.en_US
dc.identifier.citedreferenceHuang, X., Atwood, C. S., Hartshorn, M. A., Multhaup, G., Goldstein, L. E., Scarpa, R. C., Cuajungco, M. P., Gray, D. N., Lim, J., Moir, R. D., Tanzi, R. E., and Bush, A. I. ( 1999 ) The A β peptide of Alzheimer's disease directly produces hydrogen peroxide through metal ion reduction. Biochemistry 38, 7609 – 7616.en_US
dc.identifier.citedreferenceNelson, T. J. and Alkon, D. L. ( 2005 ) Oxidation of cholesterol by amyloid precursor protein and β‐amyloid peptide. J. Biol. Chem. 280, 7377 – 7387.en_US
dc.identifier.citedreferenceMulthaup, G., Schlicksupp, A., Hesse, L., Beher, D., Ruppert, T., Masters, C. L., and Beyreuther, K. ( 1996 ) The amyloid precursor protein of Alzheimer's disease in the reduction of copper(II) to copper(I). Science 271, 1406 – 1409.en_US
dc.identifier.citedreferenceWhite, A. R., Multhaup, G., Galatis, D., McKinstry, W. J., Parker, M. W., Pipkorn, R., Beyreuther, K., Masters, C. L., and Cappai, R. ( 2002 ) Contrasting, species‐dependent modulation of copper‐mediated neurotoxicity by the Alzheimer's disease amyloid precursor protein. J. Neurosci. 22, 365 – 376.en_US
dc.identifier.citedreferenceMa, Q., Li, Y., Du, J., Liu, H., Kanazawa, K., Nemoto, T., Nakanishi, H., and Zhao, Y. ( 2006 ) Copper binding properties of a tau peptide associated with Alzheimer's disease studied by CD, NMR, and MALDI‐TOF MS. Peptides 27, 841 – 849.en_US
dc.identifier.citedreferenceNakano, E., Williamson, M. P., Williams, N. H., and Powers, H. J. ( 2004 ) Copper‐mediated LDL oxidation by homocysteine and related compounds depends largely on copper ligation. Biochim. Biophys. Acta 1688, 33 – 42.en_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


Files in this item

Name:
1005_ftp.pdf
Size:
740.3KB
Format:
PDF
View/Open

Show simple item record

Remediation of Harmful Language

The University of Michigan Library aims to describe library materials in a way that respects the people and communities who create, use, and are represented in our collections. Report harmful or offensive language in catalog records, finding aids, or elsewhere in our collections anonymously through our metadata feedback form. More information at Remediation of Harmful Language.

Accessibility

If you are unable to use this file in its current format, please select the Contact Us link and we can modify it to make it more accessible to you.