Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2010 Jul 18:2010:180734.
doi: 10.4061/2010/180734.

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

Radmila Mileusnic  1 , Steven Rose
Affiliations

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

Radmila Mileusnic et al. Int J Alzheimers Dis. .

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.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Alignment of the amino acid sequences of human, mouse, and chick APP. The numbering refers to the human APP sequence. The RERMS sequence is in gray. Amino acid sequences of Aβ domain are underlined. Residues implicated in amyloidogenesis are indicated in bold. The human (P05067), chicken (Q9DGJ7) and mouse (P12023) APP sequences were obtained from the EMBL database (CLUSTAL 2.0.12 multiple sequence alignment).
Figure 2
Figure 2
Two time-windows when protein synthesis is sensitive to inhibitors of protein synthesis, such as anisomycin (ANI) and glycoprotein synthesis, such as 2-d-Galactose (2-d-Gal).
Figure 3
Figure 3
RER binding detected on chick, human and mouse neuronal cells. Specific binding of the biotinylated RER (arrows) to chick (a), human (b) and mouse neuronal (c) cell. Location of the chick neuronal cells is in the IMMP area; Human and mouse neuronal cells are located in the CA1 are in hippocampus.
Figure 4
Figure 4
Structure of D/L tripeptides included in the study.
See this image and copyright information in PMC

References

    1. Porsolt RD. Animal models of depression: utility for transgenic research. Reviews in the Neurosciences. 2000;11(1):53–58. - PubMed
    1. Kalueff AV, Wheaton M, Murphy DL. What's wrong with my mouse model? Advances and strategies in animal modeling of anxiety and depression. Behavioural Brain Research. 2007;179(1):1–18. - PubMed
    1. Fujii T, Kunugi H. p75NTR as a therapeutic target for neuropsychiatric diseases. Current Molecular Pharmacology. 2009;2(1):70–76. - PubMed
    1. Moisan MP, Ramos A. Rat genomics applied to psychiatric research. Methods in Molecular Biology. 2010;597:357–388. - PubMed
    1. Hart PC, Bergner CL, Smolinsky AN, et al. Experimental models of anxiety for drug discovery and brain research. Methods in Molecular Biology. 2010;602:299–321. - PubMed

LinkOut - more resources