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International Journal of Alzheimer’s Disease
Volume 2014, Article ID 483281, 7 pages
http://dx.doi.org/10.1155/2014/483281
Research Article

Neprilysin Is Poorly Expressed in the Prefrontal Cortex of Aged Dogs with Cognitive Dysfunction Syndrome

1Araclon Biotech Ltd., Vía Hispanidad 21, 50009 Zaragoza, Spain
2Departamento de Ciencias Clínicas Veterinarias, Facultad de Veterinaria de Lugo, Universidad de Santiago de Compostela, 27002 Lugo, Spain

Received 1 October 2013; Revised 16 December 2013; Accepted 21 December 2013; Published 6 January 2014

Academic Editor: Mark Kindy

Copyright © 2014 Jesús Canudas et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Linked References

  1. J. A. Hardy and G. A. Higgins, “Alzheimer's disease: the amyloid cascade hypothesis,” Science, vol. 256, no. 5054, pp. 184–185, 1992. View at Google Scholar · View at Scopus
  2. J. Hardy and D. J. Selkoe, “The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics,” Science, vol. 297, no. 5580, pp. 353–356, 2002. View at Publisher · View at Google Scholar · View at Scopus
  3. N. Iwata, M. Higuchi, and T. C. Saido, “Metabolism of amyloid-β peptide and Alzheimer's disease,” Pharmacology and Therapeutics, vol. 108, no. 2, pp. 129–148, 2005. View at Publisher · View at Google Scholar · View at Scopus
  4. N. Iwata, S. Tsubuki, Y. Takaki et al., “Metabolic regulation of brain Aβ by neprilysin,” Science, vol. 292, no. 5521, pp. 1550–1552, 2001. View at Publisher · View at Google Scholar · View at Scopus
  5. H. Kanemitsu, T. Tomiyama, and H. Mori, “Human neprilysin is capable of degrading amyloid β peptide not only in the monomeric form but also the pathological oligomeric form,” Neuroscience Letters, vol. 350, no. 2, pp. 113–116, 2003. View at Publisher · View at Google Scholar · View at Scopus
  6. C. Li, R. M. Booze, and L. B. Hersh, “Tissue-specific expression of rat neutral endopeptidase (neprilysin) mRNAs,” Journal of Biological Chemistry, vol. 270, no. 11, pp. 5723–5728, 1995. View at Publisher · View at Google Scholar · View at Scopus
  7. C. E. Reilly, “Neprilysin content is reduced in Alzheimer brain areas,” Journal of Neurology, vol. 248, no. 2, pp. 159–160, 2001. View at Publisher · View at Google Scholar · View at Scopus
  8. K. Yasojima, E. G. McGeer, and P. L. McGeer, “Relationship between beta amyloid peptide generating molecules and neprilysin in Alzheimer disease and normal brain,” Brain Research, vol. 919, no. 1, pp. 115–121, 2001. View at Publisher · View at Google Scholar · View at Scopus
  9. A. Caccamo, S. Oddo, M. C. Sugarman, Y. Akbari, and F. M. LaFerla, “Age- and region-dependent alterations in Aβ-degrading enzymes: implications for Aβ-induced disorders,” Neurobiology of Aging, vol. 26, no. 5, pp. 645–654, 2005. View at Publisher · View at Google Scholar · View at Scopus
  10. N. Iwata, Y. Takaki, S. Fukami, S. Tsubuki, and T. C. Saido, “Region-specific reduction of Aβ-degrading endopeptidase, neprilysin, in mouse hippocampus upon aging,” Journal of Neuroscience Research, vol. 70, no. 3, pp. 493–500, 2002. View at Publisher · View at Google Scholar · View at Scopus
  11. E. Hellström-Lindahl, R. Ravid, and A. Nordberg, “Age-dependent decline of neprilysin in Alzheimer's disease and normal brain: inverse correlation with Aβ levels,” Neurobiology of Aging, vol. 29, no. 2, pp. 210–221, 2008. View at Publisher · View at Google Scholar · View at Scopus
  12. J. S. Miners, Z. van Helmond, P. G. Kehoe, and S. Love, “Changes with age in the activities of β-secretase and the aβ-degrading enzymes neprilysin, insulin-degrading enzyme and angiotensin-converting enzyme,” Brain Pathology, vol. 20, no. 4, pp. 794–802, 2010. View at Publisher · View at Google Scholar · View at Scopus
  13. R. Poirier, D. P. Wolfer, H. Welzl et al., “Neuronal neprilysin overexpression is associated with attenuation of Aβ-related spatial memory deficit,” Neurobiology of Disease, vol. 24, no. 3, pp. 475–483, 2006. View at Publisher · View at Google Scholar · View at Scopus
  14. J. S. Miners, N. Barua, P. G. Kehoe, S. Gill, and S. Love, “Aβ-degrading enzymes: potential for treatment of alzheimer disease,” Journal of Neuropathology and Experimental Neurology, vol. 70, no. 11, pp. 944–959, 2011. View at Publisher · View at Google Scholar · View at Scopus
  15. B. J. Cummings, E. Head, A. J. Afagh, N. W. Milgram, and C. W. Cotman, “β-amyloid accumulation correlates with cognitive dysfunction in the aged canine,” Neurobiology of Learning and Memory, vol. 66, no. 1, pp. 11–23, 1996. View at Publisher · View at Google Scholar · View at Scopus
  16. E. Head, “Combining an antioxidant-fortified diet with behavioral enrichment leads to cognitive improvement and reduced brain pathology in aging canines: strategies for healthy aging,” Annals of the New York Academy of Sciences, vol. 1114, pp. 398–406, 2007. View at Publisher · View at Google Scholar · View at Scopus
  17. D. Insua, A. Corredoira, Á. González-Martínez et al., “Expression of p75NTR, a marker for basal forebrain cholinergic neurons, in young and aged dogs with or without cognitive dysfunction syndrome,” Journal of Alzheimer's Disease, vol. 28, no. 2, pp. 291–296, 2012. View at Publisher · View at Google Scholar · View at Scopus
  18. D. Insua, M.-L. Suárez, G. Santamarina, M. Sarasa, and P. Pesini, “Dogs with canine counterpart of Alzheimer's disease lose noradrenergic neurons,” Neurobiology of Aging, vol. 31, no. 4, pp. 625–635, 2010. View at Publisher · View at Google Scholar · View at Scopus
  19. W. O. Opii, G. Joshi, E. Head et al., “Proteomic identification of brain proteins in the canine model of human aging following a long-term treatment with antioxidants and a program of behavioral enrichment: relevance to Alzheimer's disease,” Neurobiology of Aging, vol. 29, no. 1, pp. 51–70, 2008. View at Publisher · View at Google Scholar · View at Scopus
  20. M. Sarasa and P. Pesini, “Natural non-trasgenic animal models for research in alzheimer's disease,” Current Alzheimer Research, vol. 6, no. 2, pp. 171–178, 2009. View at Publisher · View at Google Scholar · View at Scopus
  21. C. T. Siwak-Tapp, E. Head, B. A. Muggenburg, N. W. Milgram, and C. W. Cotman, “Region specific neuron loss in the aged canine hippocampus is reduced by enrichment,” Neurobiology of Aging, vol. 29, no. 1, pp. 39–50, 2008. View at Publisher · View at Google Scholar · View at Scopus
  22. E. M. Johnstone, M. O. Chaney, F. H. Norris, R. Pascual, and S. P. Little, “Conservation of the sequence of the Alzheimer's disease amyloid peptide in dog, polar bear and five other mammals by cross-species polymerase chain reaction analysis,” Molecular Brain Research, vol. 10, no. 4, pp. 299–305, 1991. View at Publisher · View at Google Scholar · View at Scopus
  23. L. Sarasa, C. Gallego, I. Monleón et al., “Cloning, sequencing and expression in the dog of the main amyloid precursor protein isoforms and some of the enzymes related with their processing,” Neuroscience, vol. 171, no. 4, pp. 1091–1101, 2010. View at Publisher · View at Google Scholar · View at Scopus
  24. Á. González-Martínez, B. Rosado, P. Pesini et al., “Plasma β-amyloid peptides in canine aging and cognitive dysfunction as a model of Alzheimer's disease,” Experimental Gerontology, vol. 46, no. 7, pp. 590–596, 2011. View at Publisher · View at Google Scholar · View at Scopus
  25. K. J. Livak and T. D. Schmittgen, “Analysis of relative gene expression data using real-time quantitative PCR and the 2-ΔΔCT method,” Methods, vol. 25, no. 4, pp. 402–408, 2001. View at Publisher · View at Google Scholar · View at Scopus
  26. R. Mitra, O. S. Chao, D. M. Nanus, and O. B. Goodman Jr., “Negative regulation of NEP expression by hypoxia,” Prostate, vol. 73, no. 7, pp. 706–714, 2013. View at Publisher · View at Google Scholar
  27. F. Bao, L. Wicklund, P. N. Lacor, W. L. Klein, A. Nordberg, and A. Marutle, “Different β-amyloid oligomer assemblies in Alzheimer brains correlate with age of disease onset and impaired cholinergic activity,” Neurobiology of Aging, vol. 33, no. 4, pp. 825.e1–825.e13, 2012. View at Publisher · View at Google Scholar · View at Scopus
  28. S. Fukami, K. Watanabe, N. Iwata et al., “Aβ-degrading endopeptidase, neprilysin, in mouse brain: synaptic and axonal localization inversely correlating with Aβ pathology,” Neuroscience Research, vol. 43, no. 1, pp. 39–56, 2002. View at Publisher · View at Google Scholar · View at Scopus
  29. M. P. Lambert, A. K. Barlow, B. A. Chromy et al., “Diffusible, nonfibrillar ligands derived from Aβ1-42 are potent central nervous system neurotoxins,” Proceedings of the National Academy of Sciences of the United States of America, vol. 95, no. 11, pp. 6448–6453, 1998. View at Google Scholar · View at Scopus
  30. C. Haass and D. J. Selkoe, “Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid β-peptide,” Nature Reviews Molecular Cell Biology, vol. 8, no. 2, pp. 101–112, 2007. View at Publisher · View at Google Scholar · View at Scopus