Journal article
Spatial memory deficits in a mouse model of late-onset Alzheimer's disease are caused by zinc supplementation and correlate with amyloid-beta levels
JM Flinn, P Lorenzo Bozzelli, PA Adlard, AM Railey
Frontiers in Aging Neuroscience | Published : 2014
Abstract
Much of the research in Alzheimer's disease (AD) that uses mouse models focuses on the early-onset form of the disease, which accounts for less than 5% of cases. In contrast, this study used a late-onset AD model to examine the interaction between increased dietary zinc (Zn) and the apolipoprotein E (ApoE) gene. ApoE e4 is overrepresented in late-onset AD and enhances Zn binding to amyloid-ß (Aß). This study sought to determine if elevated dietary Zn would impair spatial memory in CRND8 mice (CRND8), as well as mice who carry both the mutated human APP and ApoE e4 genes (CRND8/E4). Mice were provided with either lab tap water or water enhanced with 10 ppm Zn (ZnCO3) for 4 months. At 6 months..
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Funding Acknowledgements
The authors would like to thank Lara Glenn for assistance with many aspects of the study, Kathy Conko of USGS for analyzing water samples, Caroline L. C. Neely for manuscript edits, the University of Toronto for donating the CRND8 mice, and the reviewers of this manuscript for their helpful comments. This research was funded in part by a Sigma Xi GIAR and an APA dissertation research award to Angela M. Railey. Paul Anthony Adlard is supported by the NHMRC and ARC. In addition, the Florey Institute of Neuroscience and Mental Health acknowledges the strong support from the Victorian Government and in particular the funding from the Operational Infrastructure Support Grant. Publication of this article was funded in part by the George Mason University Libraries Open Access Fund.