13 Brenner S. The genetics of Caenorhabditis elegans. Genetics, 1974, 77: 71-94
[2]
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？？
[3]
15 Cohen E, Bieschke J, Perciavalle R M, et al. Opposing activities protect against age-onset proteotoxicity. Science, 2006, 313: 1604-1610？？
[4]
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？？
[5]
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？？
[6]
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？？
[7]
19 Praticò D. Oxidative stress hypothesis in Alzheimer’s disease: a reappraisal. Trends Pharmacol Sci, 2008, 29: 609-615？？
[8]
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
[9]
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？？
[10]
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？？
[11]
29 Good P F, Werner P, Hsu A, et al. Evidence for neuronal oxidative damage in Alzheimer’s disease. Am J of Pathol, 1996, 149: 21
[12]
30 Markesbery W R, Carney J M. Oxidative alterations in Alzheimer’s disease. Brain Pathol, 1999, 9: 133-146
[13]
31 Smith M A, Rottkamp C A, Nunomura A, et al. Oxidative stress in Alzheimer’s disease. Biochim Biophys Acta, 2000, 1502: 139-144
[14]
32 Zhu X, Raina A K, Perry G, et al. Alzheimer’s disease: the two-hit hypothesis. Lancet Neurol, 2004, 3: 219-226？？
[15]
33 Perry G, Nunomura A, Hirai K, et al. Is oxidative damage the fundamental pathogenic mechanism of Alzheimer’s and other neurodegenerative diseases? Free Radic Biol Medi, 2002, 11: 1475-1479
[16]
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 ？？
[17]
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 ？？
[18]
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
[19]
1 Mattson M P. Pathways towards and away from Alzheimer’s disease. Nature, 2004, 430: 631-639？？
[20]
2 Goedert M, Spillantini M G. A century of Alzheimer’s disease. Science, 2006, 314: 777-781？？
[21]
3 Bush A I. The metallobiology of Alzheimer’s disease. Trends Neurosci, 2003, 26: 207-214？？
[22]
4 Bush A I, Curtain C C. Twenty years of metallo-neurobiology: where to now? Eur Biophys J, 2007, 37: 241-245
[23]
5 Cater M A, McInnes K T, Li Q X, et al. Intracellular copper deficiency increases amyloid-beta secretion by diverse mechanisms. Biochem J, 2008, 412: 141-152？？
[24]
6 Crouch P J, Hung L W, Adlard P A, et al. Increasing Cu bioavailability inhibits Abeta oligomers and tau phosphorylation. Proc Natl Acad Sci USA, 2009, 106: 381-386？？
[25]
7 Markesbery W R. Oxidative stress hypothesis in Alzheimer’s disease. Free Radic Biol Med, 1997, 23: 134-147？？
[26]
8 Sparks D L, Schreurs B G. Trace amounts of copper in water induce beta-amyloid plaques and learning deficits in a rabbit model of Alzheimer’s disease. Proc Natl Acad Sci USA, 2003, 100: 11065-11069？？
[27]
9 Phinney A L, Drisaldi B, Schmidt S D, et al. In vivo reduction of amyloid-beta by a mutant copper transporter. Proc Natl Acad Sci USA, 2003, 100: 14193-14198 ？？
[28]
10 Bayer T A, Sch?fer S, Simons A, et al. Dietary Cu stabilizes brain superoxide dismutase 1 activity and reduces amyloid Abeta production in APP23 transgenic mice. Proc Natl Acad Sci USA , 2003, 100: 14187-14192？？
[29]
11 Link C D. Invertebrate models of Alzheimer’s disease. Genes Brain Behav, 2005, 4: 147-156？？
[30]
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？？
[31]
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
[32]
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？？
[33]
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？？
[34]
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？？
[35]
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？？
[36]
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？？
