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Journal of Biomedicine and Biotechnology
Volume 2011 (2011), Article ID 617974, 12 pages
http://dx.doi.org/10.1155/2011/617974
Research Article

Presenilin-2 Mutation Causes Early Amyloid Accumulation and Memory Impairment in a Transgenic Mouse Model of Alzheimer's Disease

1Molecular Gerontology, Tokyo Metropolitan Institute of Gerontology, 35-2 Sakae-Cho, Itabashi-Ku, Tokyo 173-0015, Japan
2JAC Co, Ltd, 1-2-7 Higashiyama, Meguro-Ku, Tokyo 153-0043, Japan
3Immuno-Biological Laboratories Co, Ltd., 1091-1 Naka, Aza-Higashida, Fujioka-shi, Gunma 370-0831, Japan

Received 15 September 2010; Revised 17 November 2010; Accepted 4 December 2010

Academic Editor: Monica Fedele

Copyright © 2011 Toshihiko Toda 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. D. J. Selkoe, “Developing preventive therapies for chronic diseases: lessons learned from Alzheimer's disease,” Nutrition reviews, vol. 65, part 2, pp. S239–243, 2007. View at Scopus
  2. 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 PubMed · View at Scopus
  3. A. Aguzzi and T. O'Connor, “Protein aggregation diseases: pathogenicity and therapeutic perspectives,” Nature Reviews Drug Discovery, vol. 9, no. 3, pp. 237–248, 2010. View at Publisher · View at Google Scholar · View at PubMed · View at Scopus
  4. J. Hardy, “The Alzheimer family of diseases: many etiologies, one pathogenesis?” Proceedings of the National Academy of Sciences of the United States of America, vol. 94, no. 6, pp. 2095–2097, 1997. View at Publisher · View at Google Scholar · View at Scopus
  5. D. L. Price and S. S. Sisodia, “Mutant genes in familial Alzheimer's disease and transgenic models,” Annual Review of Neuroscience, vol. 21, pp. 479–505, 1998. View at Publisher · View at Google Scholar · View at PubMed · View at Scopus
  6. C. Janus and D. Westaway, “Transgenic mouse models of Alzheimer's disease,” Physiology and Behavior, vol. 73, no. 5, pp. 873–886, 2001. View at Publisher · View at Google Scholar · View at Scopus
  7. G. A. Higgins and H. Jacobsen, “Transgenic mouse models of Alzheimer's disease: phenotype and application,” Behavioural Pharmacology, vol. 14, no. 5-6, pp. 419–438, 2003. View at Scopus
  8. D. Games, D. Adams, R. Alessandrini et al., “Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein,” Nature, vol. 373, no. 6514, pp. 523–527, 1995. View at Scopus
  9. K. Hsiao, P. Chapman, S. Nilsen et al., “Correlative memory deficits, Aβ elevation, and amyloid plaques in transgenic mice,” Science, vol. 274, no. 5284, pp. 99–102, 1996. View at Publisher · View at Google Scholar · View at Scopus
  10. C. Sturchler-Pierrat, D. Abramowski, M. Duke et al., “Two amyloid precursor protein transgenic mouse models with Alzheimer disease-like pathology,” Proceedings of the National Academy of Sciences of the United States of America, vol. 94, no. 24, pp. 13287–13292, 1997. View at Publisher · View at Google Scholar · View at Scopus
  11. M. A. Chishti, D. S. Yang, C. Janus et al., “Early-onset Amyloid Deposition and Cognitive Deficits in Transgenic Mice Expressing a Double Mutant Form of Amyloid Precursor Protein 695,” Journal of Biological Chemistry, vol. 276, no. 24, pp. 21562–21570, 2001. View at Publisher · View at Google Scholar · View at PubMed · View at Scopus
  12. M. A. Westerman, D. Cooper-Blacketer, A. Mariash et al., “The relationship between Aβ and memory in the Tg2576 mouse model of Alzheimer's disease,” Journal of Neuroscience, vol. 22, no. 5, pp. 1858–1867, 2002. View at Scopus
  13. M. N. Gordon, D. L. King, D. M. Diamond et al., “Correlation between cognitive deficits and Aβ deposits in transgenic APP+PS1 mice,” Neurobiology of Aging, vol. 22, no. 3, pp. 377–385, 2001. View at Publisher · View at Google Scholar · View at Scopus
  14. E. I. Rogaev, R. Sherrington, E. A. Rogaeva et al., “Familial Alzheimer's disease in kindreds with missense mutations in a gene on chromosome 1 related to the Alzheimer's disease type 3 gene,” Nature, vol. 376, no. 6543, pp. 775–778, 1995. View at Scopus
  15. G. Marcon, G. Giaccone, C. Cupidi et al., “Neuropathological and clinical phenotype of an Italian Alzheimer family with M239V mutation of presenilin 2 gene,” Journal of Neuropathology and Experimental Neurology, vol. 63, no. 3, pp. 199–209, 2004. View at Scopus
  16. N. Sawamura, M. Morishima-Kawashima, H. Waki et al., “Mutant presenilin 2 transgenic mice: a large increase in the levels of Aβ342 is presumably associated with the low density membrane domain that contains decreased levels of glycerophospholipids and sphingomyelin,” Journal of Biological Chemistry, vol. 275, no. 36, pp. 27901–27908, 2000. View at Publisher · View at Google Scholar · View at PubMed · View at Scopus
  17. F. Oyama, N. Sawamura, K. Kobayashi et al., “Mutant presenilin 2 transgenic mouse: effect on an age-dependent increase of amyloid β-protein 42 in the brain,” Journal of Neurochemistry, vol. 71, no. 1, pp. 313–322, 1998. View at Scopus
  18. R. Morris, “Developments of a water-maze procedure for studying spatial learning in the rat,” Journal of Neuroscience Methods, vol. 11, no. 1, pp. 47–60, 1984. View at Publisher · View at Google Scholar · View at Scopus
  19. E. Ognibene, S. Middei, S. Daniele et al., “Aspects of spatial memory and behavioral disinhibition in Tg2576 transgenic mice as a model of Alzheimer's disease,” Behavioural Brain Research, vol. 156, no. 2, pp. 225–232, 2005. View at Publisher · View at Google Scholar · View at PubMed · View at Scopus
  20. M. Tabuchi, T. Yamaguchi, S. Iizuka, S. Imamura, Y. Ikarashi, and Y. Kase, “Ameliorative effects of yokukansan, a traditional Japanese medicine, on learning and non-cognitive disturbances in the Tg2576 mouse model of Alzheimer's disease,” Journal of Ethnopharmacology, vol. 122, no. 1, pp. 157–162, 2009. View at Publisher · View at Google Scholar · View at PubMed · View at Scopus
  21. N. R. Rustay, E. A. Cronin, P. Curzon et al., “Mice expressing the Swedish APP mutation on a 129 genetic background demonstrate consistent behavioral deficits and pathological markers of Alzheimer's disease,” Brain Research, vol. 1311, pp. 136–147, 2010. View at Publisher · View at Google Scholar · View at PubMed · View at Scopus
  22. T. Iwatsubo, D. M. A. Mann, A. Odaka, N. Suzuki, and Y. Ihara, “Amyloid β protein (Aβ) deposition: Aβ42(43) precedes Aβ40 in Down syndrome,” Annals of Neurology, vol. 37, no. 3, pp. 294–299, 1995. View at Publisher · View at Google Scholar · View at PubMed · View at Scopus
  23. T. Tomita, K. Maruyama, T. C. Saido et al., “The presenilin 2 mutation (N141I) linked to familial Alzheimer disease (Volga German families) increases the secretion of amyloid β protein ending at the 42nd (or 43rd) residue,” Proceedings of the National Academy of Sciences of the United States of America, vol. 94, no. 5, pp. 2025–2030, 1997. View at Publisher · View at Google Scholar · View at Scopus
  24. R. M. Page, K. Baumann, M. Tomioka et al., “Generation of Aβ38 and Aβ42 is independently and differentially affected by familial Alzheimer disease-associated presenilin mutations and γ-secretase modulation,” Journal of Biological Chemistry, vol. 283, no. 2, pp. 677–683, 2008. View at Publisher · View at Google Scholar · View at PubMed
  25. C. A. Saura, “Presenilin/gamma-secretase and inflammation,” Frontiers in Aging Neuroscience, vol. 2, p. 16, 2010.
  26. B. De Strooper, “Loss-of-function presenilin mutations in Alzheimer disease. Talking Point on the role of presenilin mutations in Alzheimer disease,” EMBO Reports, vol. 8, no. 2, pp. 141–146, 2007. View at Publisher · View at Google Scholar · View at PubMed · View at Scopus
  27. K. Duff, C. Eckman, C. Zehr et al., “Increased amyloid-β42(43) in brains of mice expressing mutant presenilin 1,” Nature, vol. 383, no. 6602, pp. 710–713, 1996. View at Publisher · View at Google Scholar · View at PubMed
  28. J. G. Richards, G. A. Higgins, A. M. Ouagazzal et al., “PS2APP transgenic mice, coexpressing hPS2mut and hAPPswe, show age-related cognitive deficits associated with discrete brain amyloid deposition and inflammation,” Journal of Neuroscience, vol. 23, no. 26, pp. 8989–9003, 2003.
  29. C. L. Maarouf, I. D. Daugs, S. Spina et al., “Histopathological and molecular heterogeneity among individuals with dementia associated with Presenilin mutations,” Molecular Neurodegeneration, vol. 3, no. 1, article 20, 2008. View at Publisher · View at Google Scholar · View at PubMed
  30. J. Maeda, B. Ji, T. Irie et al., “Longitudinal, quantitative assessment of amyloid, neuroinflammation, and anti-amyloid treatment in a living mouse model of Alzheimer's disease enabled by positron emission tomography,” Journal of Neuroscience, vol. 27, no. 41, pp. 10957–10968, 2007. View at Publisher · View at Google Scholar · View at PubMed
  31. J. C. Price, W. E. Klunk, B. J. Lopresti et al., “Kinetic modeling of amyloid binding in humans using PET imaging and Pittsburgh Compound-B,” Journal of Cerebral Blood Flow and Metabolism, vol. 25, no. 11, pp. 1528–1547, 2005. View at Publisher · View at Google Scholar · View at PubMed