Copper ions influence the toxicity of β-amyloid(1-42) in a concentration-dependent manner in a Caenorhabditis elegans model of Alzheimer's disease

Science China Life Sciences

Volumn 54, Issue 6, 2011, Pages 527-534

  Luo, Yun Feng ^a,b   Zhang, Jie ^c   Liu, Nian Qing ^d   Luo, Yuan ^e   Zhao, Bao Lu ^a  

^a INSTITUTE OF BIOPHYSICS   (China)

^b UNIVERSITY OF CHINESE ACADEMY OF SCIENCES   (China)

^c RUTGERS UNIVERSITY   (United States)

^d INSTITUTE OF HIGH ENERGY PHYSICS   (China)

^e UNIVERSITY OF MARYLAND   (United States)

Author keywords

amyloid(1 42); Alzheimer's disease; C. elegans; copper; oxidative stress

Indexed keywords

AMYLOID BETA PROTEIN; AMYLOID BETA PROTEIN (1 42); AMYLOID BETA-PROTEIN (1-42); CAENORHABDITIS ELEGANS PROTEIN; COPPER; ION; PEPTIDE FRAGMENT; REACTIVE OXYGEN METABOLITE;

ALZHEIMER DISEASE; ANIMAL; ARTICLE; CAENORHABDITIS ELEGANS; CHEMICALLY INDUCED DISORDER; DISEASE MODEL; DOSE RESPONSE; DRUG EFFECT; GENE EXPRESSION; GENETICS; HOMEOSTASIS; METABOLISM; OXIDATIVE STRESS; PARALYSIS; PHYSIOLOGY; SYNCHROTRON; TRANSGENIC ANIMAL;

ALZHEIMER DISEASE; AMYLOID BETA-PEPTIDES; ANIMALS; ANIMALS, GENETICALLY MODIFIED; CAENORHABDITIS ELEGANS; CAENORHABDITIS ELEGANS PROTEINS; COPPER; DISEASE MODELS, ANIMAL; DOSE-RESPONSE RELATIONSHIP, DRUG; GENE EXPRESSION; HOMEOSTASIS; IONS; OXIDATIVE STRESS; PARALYSIS; PEPTIDE FRAGMENTS; REACTIVE OXYGEN SPECIES; SYNCHROTRONS;

CAENORHABDITIS ELEGANS;

EID: 79959613455     PISSN: 16747305     EISSN: None     Source Type: Journal    
DOI: 10.1007/s11427-011-4180-z     Document Type: Article

References (36)

1. Mattson M P. Pathways towards and away from Alzheimer's disease. Nature, 2004, 430: 631-639.
2. Goedert M, Spillantini M G. A century of Alzheimer's disease. Science, 2006, 314: 777-781.
3. Bush A I. The metallobiology of Alzheimer's disease. Trends Neurosci, 2003, 26: 207-214.
4. Bush A I, Curtain C C. Twenty years of metallo-neurobiology: Where to now? Eur Biophys J, 2007, 37: 241-245.
5. Cater M A, McInnes K T, Li Q X, et al. Intracellular copper deficiency increases amyloid-β secretion by diverse mechanisms. Biochem J, 2008, 412: 141-152.
6. Crouch P J, Hung L W, Adlard P A, et al. Increasing Cu bioavailability inhibits Aβ oligomers and tau phosphorylation. Proc Natl Acad Sci USA, 2009, 106: 381-386.
7. Markesbery W R. Oxidative stress hypothesis in Alzheimer's disease. Free Radical Bio Med, 2007, 23: 134-147.
8. Sparks D L, Schreurs B G. 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, 2003, 100: 11065-11069.
9. Phinney A L, Drisaldi B, Schmidt S D, et al. In vivo reduction of amyloid-β by a mutant copper transporter. Proc Natl Acad Sci USA, 2003, 100: 14193-14198.
10. Bayer T A, Schäfer S, Simons A, et al. Dietary Cu stabilizes brain superoxide dismutase 1 activity and reduces amyloid Aβ production in APP23 transgenic mice. Proc Natl Acad Sci USA, 2003, 100: 14187-14192.
11. Link C D. Invertebrate models of Alzheimer's disease. Genes Brain Behav, 2005, 4: 147-156.
12. Link C D. C. elegans models of age-associated neurodegenerative diseases: Lessons from transgenic worm models of Alzheimer's disease. Exp Gerontol, 2006, 41: 1007-1013.
13. Brenner S. The genetics of Caenorhabditis elegans. Genetics, 1974, 77: 71-94.
14. Feng Z, Li W, Ward A, et al. A C. elegans model of nicotine-dependent behavior: Regulation by TRP-family channels. Cell, 2006, 127: 621-633.
15. Cohen E, Bieschke J, Perciavalle R M, et al. Opposing activities protect against age-onset proteotoxicity. Science, 2006, 313: 1604-1610.
16. Gao Y X, Liu N Q, Chen C Y, et al. Mapping technique for biodistribution of elements in a model organism, Caenorhabditis elegans, after exposure to copper nanoparticles with microbeam synchrotron radiation X-ray fluorescence. J Anal At Spectrom, 2008, 23: 1121-1124.
17. Schulz T J, Zarse K, Voigt A, et al. Glucose restriction extends Caenorhabditis elegans life span by inducing mitochondrial respiration and increasing oxidative stress. Cell Metab, 2007, 6: 280-293.
18. Hoogewijs D, Houthoofd K, Matthijssens F, et al. Selection and validation of a set of reliable reference genes for quantitative sod gene expression analysis in C. elegans. BMC Mol Biol, 2008, 9: 9.
19. Praticò D. Oxidative stress hypothesis in Alzheimer's disease: A reappraisal. Trends Pharmacol Sci, 2008, 29: 609-615.
20. Giglio A M, Hunter T, Bannister J V, et al. The copper/zinc superoxide dismutase gene of Caenorhabditis elegans. Biochem Mol Biol Int, 1994, 33: 41-44.
21. Hunter T, Bannister W H, Hunter G J. Cloning, expression, and characterization of two manganese superoxide dismutases from Caenorhabditis elegans. J Biol Chem, 1997, 272: 28652-28659.
22. Taub J, Lau J F, Ma C, et al. A cytosolic catalase is needed to extend adult lifespan in C. elegans daf-C and clk-1 mutants. Nature, 1999, 399: 162-166.
23. Isermann K, Liebau E, Roeder T, et al. A peroxiredoxin specifically expressed in two types of pharyngeal neurons is required for normal growth and egg production in Caenorhabditis elegans. J Mol Biol, 2004, 338: 745-755.
24. Simonetta S H, Romanowski A, Minniti A N, et al. Circadian stress tolerance in adult Caenorhabditis elegans. J Comp Physiol A Neuroethol Sens Neural Behav Physiol, 2008, 194: 821-828.
25. An J H, Vranas K, Lucke M, et al. Regulation of the Caenorhabditis elegans oxidative stress defense protein SKN-1 by glycogen synthase kinase-3. Proc Natl Acad Sci USA, 2005, 102: 16275-16280.
26. Steinkraus K A, Smith E D, Davis C, et al. Dietary restriction suppresses proteotoxicity and enhances longevity by an hsf-1-dependent mechanism in Caenorhabditis elegans. Aging Cell, 2008, 7: 394-404.
27. Benedetti C, Haynes C M, Yang Y, et al. Ubiquitin-like protein 5 positively regulates chaperone gene expression in the mitochondrial unfolded protein response. Genetics, 2006, 174: 229-239.
28. Hong M, Kwon J Y, Shim J, et al. Differential hypoxia response of hsp-16 genes in the nematode. J Mol Biol, 2004, 344: 369-381.
29. Good P F, Werner P, Hsu A, et al. Evidence for neuronal oxidative damage in Alzheimer's disease. Am J Pathol, 1996, 149: 21.
30. Markesbery W R, Carney J M. Oxidative alterations in Alzheimer's disease. Brain Pathology, 1999, 9: 133-146.
31. Smith M A, Rottkamp C A, Nunomura A, et al. Oxidative stress in Alzheimer's disease. Biochim Biophys Acta-Mol Basis Dis, 2000, 1502: 139-144.
32. Zhu X, Raina A K, Perry G, et al. Alzheimer's disease: The two-hit hypothesis. Lancet Neurol, 2004, 3: 219-226.
33. Perry G, Nunomura A, Hirai K, et al. Is oxidative damage the fundamental pathogenic mechanism of Alzheimer's and other neurodegenerative diseases? Free Radical Bio Med, 2002, 11: 1475-1479.
34. Lovell M A, Robertson J D, Teesdale W J, et al. Copper, iron and zinc in Alzheimer's disease senile plaques. J Neurol Sci, 1998, 158: 47-52.
35. Huang X, Cuajungco M P, Atwood C S, et al. Cu(II) potentiation of Alzheimer Aβ neurotoxicity. Correlation with cell-free hydrogen peroxide production and metal reduction. J Biol Chem, 1999, 274: 37111-37116.
36. Quinn J F, Crane S, Harris C, et al. Copper in Alzheimer's disease: Too much or too little? Expert Rev Neurother, 2009, 9: 631-637.