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

Mileusnic, Radmila and Rose, Steven (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 (In Press).

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DOI (Digital Object Identifier) Link: http://dx.doi.org/10.4061/2010/180734
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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.

Item Type: Journal Article
Copyright Holders: 2010 The Authors
ISSN: 2090-0252
Extra Information: Special issue on "Animal Models of Alzheimer's Disese".

The journal in which this paper is published is an Open Access journal. The final published version can therefore be accessed for free via the above URL.
Keywords: memory; Alzheimer's Disease; chicks; peptides; RER
Academic Unit/Department: Science > Life, Health and Chemical Sciences
Interdisciplinary Research Centre: Biomedical Research Network (BRN)
Item ID: 22355
Depositing User: Radmila Mileusnic
Date Deposited: 21 Jul 2010 11:15
Last Modified: 30 Oct 2014 19:42
URI: http://oro.open.ac.uk/id/eprint/22355
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