Display options
Cite
Mileusnic R, Rose S. The chick as a model for the study of the cellular mechanisms and potential therapies for Alzheimer's disease. Int J Alzheimers Dis. 2010;2010doi: 10.4061/2010/180734.
Mileusnic, R., & Rose, S. (2010). The chick as a model for the study of the cellular mechanisms and potential therapies for Alzheimer's disease. International journal of Alzheimer's disease, 2010. https://doi.org/10.4061/2010/180734
Mileusnic, Radmila, and Rose, Steven. "The chick as a model for the study of the cellular mechanisms and potential therapies for Alzheimer's disease." International journal of Alzheimer's disease vol. 2010 (2010). doi: https://doi.org/10.4061/2010/180734
Mileusnic R, Rose S. The chick as a model for the study of the cellular mechanisms and potential therapies for Alzheimer's disease. Int J Alzheimers Dis. 2010 Jul 18;2010. doi: 10.4061/2010/180734. PMID: 20721285; PMCID: PMC2915614.
Copy Download .nbib Format: NLM
Share it on

Int J Alzheimers Dis. 2010 Jul 18;2010. doi: 10.4061/2010/180734.

The chick as a model for the study of the cellular mechanisms and potential therapies for Alzheimer's disease.

International journal of Alzheimer's disease

Radmila Mileusnic, Steven Rose

Affiliations

  1. Department of Life Sciences, Faculty of Sciences, The Open University, Milton Keynes, MK7 6AA, UK.

PMID: 20721285 PMCID: PMC2915614 DOI: 10.4061/2010/180734

Abstract

While animal experiments have contributed much to our understanding of the mechanisms of Alzheimer's disease (AD), their value in predicting the effectiveness of treatment strategies in clinical trials has remained controversial. The disparity between the results obtained in animal models and clinical trials may in part be explained by limitations of the models and species-specific differences. We propose that one trial passive avoidance in the day-old chick is a useful system to study AD because of the close sequence homologies of chick and human amyloid precursor protein (APP). In the chick, APP is essential for memory consolidation, and disrupting its synthesis or structure results in amnesia. RER, a tripeptide sequence corresponding to part of the growth domain of APP, can restore memory loss and act as a cognitive enhancer. We suggest that RER and its homologues may form the basis for potential pharmacological protection against memory loss in AD.

References

  1. J Pharmacol Exp Ther. 2007 Mar;320(3):1144-52 - PubMed
  2. J Neurobiol. 1994 May;25(5):585-94 - PubMed
  3. Eur J Neurosci. 2004 Apr;19(7):1933-8 - PubMed
  4. Brain Res. 1994 Feb 4;636(1):162-4 - PubMed
  5. Exp Physiol. 2000 Nov;85(6):627-34 - PubMed
  6. Rev Neurosci. 2000;11(1):53-8 - PubMed
  7. Curr Alzheimer Res. 2009 Apr;6(2):171-8 - PubMed
  8. Ann Gen Psychiatry. 2007 Jun 12;6:15 - PubMed
  9. Nat Rev Neurosci. 2008 Jul;9(7):532-44 - PubMed
  10. PLoS Med. 2010 Mar 30;7(3):e1000245 - PubMed
  11. J Cell Biol. 1993 May;121(4):879-86 - PubMed
  12. Biochem Biophys Res Commun. 1989 Feb 15;158(3):906-12 - PubMed
  13. Proc Natl Acad Sci U S A. 1991 Apr 15;88(8):3363-6 - PubMed
  14. J Neurosci. 2000 Nov 1;20(21):7951-63 - PubMed
  15. Neurochem Int. 2000 Mar;36(3):175-84 - PubMed
  16. EMBO J. 1988 May;7(5):1365-70 - PubMed
  17. Neurosci Lett. 1990 Jul 17;115(1):97-102 - PubMed
  18. Behav Brain Res. 2007 Apr 16;179(1):1-18 - PubMed
  19. J Biol Chem. 1995 Nov 24;270(47):28257-67 - PubMed
  20. Nature. 2009 Oct 15;461(7266):895-7 - PubMed
  21. Learn Mem. 1995 Jan-Feb;2(1):17-25 - PubMed
  22. Brain Res. 1995 Jun 5;682(1-2):69-74 - PubMed
  23. Science. 2002 Oct 25;298(5594):789-91 - PubMed
  24. J Neurosci. 1994 Sep;14(9):5461-70 - PubMed
  25. Biochem Biophys Res Commun. 1997 Jul 9;236(1):59-65 - PubMed
  26. Annu Rev Neurosci. 1994;17:489-517 - PubMed
  27. Methods Mol Biol. 2010;602:299-321 - PubMed
  28. Cell. 1995 May 19;81(4):525-31 - PubMed
  29. Proc Natl Acad Sci U S A. 1987 Oct;84(19):6953-7 - PubMed
  30. Gene. 1993 Nov 15;133(2):255-60 - PubMed
  31. Methods Mol Biol. 2010;597:357-88 - PubMed
  32. Neuroscience. 1997 Sep;80(2):313-20 - PubMed
  33. Eur J Neurosci. 2000 Dec;12(12):4487-95 - PubMed
  34. Cell. 1994 Dec 2;79(5):755-65 - PubMed
  35. Neurobiol Learn Mem. 2004 Jan;81(1):27-38 - PubMed
  36. Brain Res. 1997 Oct 10;771(1):1-13 - PubMed
  37. Eur J Neurosci. 2003 Mar;17(5):1073-81 - PubMed
  38. Proc Natl Acad Sci U S A. 1998 Oct 13;95(21):12683-8 - PubMed
  39. Neuroscience. 2005;134(4):1285-300 - PubMed
  40. Curr Mol Pharmacol. 2009 Jan;2(1):70-6 - PubMed
  41. Brain Struct Funct. 2010 Mar;214(2-3):111-26 - PubMed
  42. Brain Res. 1996 Jan 15;706(2):181-93 - PubMed
  43. Behav Pharmacol. 2007 May;18(3):231-8 - PubMed
  44. J Neurosci. 2007 Jul 18;27(29):7817-26 - PubMed
  45. Learn Mem. 2000 Jan;7(1):1-17 - PubMed
  46. Nucleic Acids Res. 1989 Mar 11;17(5):2130 - PubMed
  47. J Inorg Biochem. 2006 May;100(5-6):952-62 - PubMed
  48. EMBO J. 2005 Dec 7;24(23):3996-4006 - PubMed
  49. Ann N Y Acad Sci. 2005 Jun;1048:149-65 - PubMed
  50. Learn Mem. 1999 Mar-Apr;6(2):120-7 - PubMed
  51. Orig Life Evol Biosph. 2002 Apr;32(2):103-27 - PubMed
  52. J Neurochem. 1995 Jun;64(6):2598-606 - PubMed
  53. J Neurobiol. 1997 May;32(5):469-80 - PubMed
  54. Brain Res Bull. 2008 Jun 15;76(3):198-207 - PubMed
  55. Alzheimers Dement. 2009 Jul;5(4):340-7 - PubMed
  56. J Neurol Neurosurg Psychiatry. 2001 Mar;70(3):323-32 - PubMed
  57. Prog Neurobiol. 2003 May;70(1):1-32 - PubMed
  58. Cereb Cortex. 1991 Jan-Feb;1(1):103-16 - PubMed
  59. Biochem Biophys Res Commun. 1987 Dec 16;149(2):665-71 - PubMed

Publication Types