A learning deficit related to age and β-amyloid plaques in a mouse model of Alzheimer's disease

Guiquan Chen, Karen S. Chen, Jane Knox, Jennifer Inglis, Andrew Bernard, Stephen J. Martin, Alan Justice, Lisa McConlogue, Dora Games, Stephen B. Freedman and Richard G. M. Morris
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Guiquan Chen: University of Edinburgh
Karen S. Chen: Elan Pharmaceuticals
Jane Knox: University of Edinburgh
Jennifer Inglis: University of Edinburgh
Andrew Bernard: University of Edinburgh
Stephen J. Martin: University of Edinburgh
Alan Justice: Elan Pharmaceuticals
Lisa McConlogue: Elan Pharmaceuticals
Dora Games: Elan Pharmaceuticals
Stephen B. Freedman: Elan Pharmaceuticals
Richard G. M. Morris: University of Edinburgh

Nature, 2000, vol. 408, issue 6815, 975-979

Abstract: Abstract Mice that overexpress the human mutant amyloid precursor protein (hAPP) show learning deficits, but the apparent lack of a relationship between these deficits and the progressive β-amyloid plaque formation that the hAPP mice display is puzzling. In the water maze1, hAPP mice are impaired before and after amyloid plaque deposition2,3,4,5,6,7. Here we show, using a new water-maze training protocol, that PDAPP mice8 also exhibit a separate age-related deficit in learning a series of spatial locations. This impairment correlates with β-amyloid plaque burden and is shown in both cross-sectional and longitudinal experimental designs. Cued navigation and object-recognition memory are normal. These findings indicate that Aβ overexpression and/or Aβ plaques are associated with disturbed cognitive function and, importantly, suggest that some but not all forms of learning and memory are suitable behavioural assays of the progressive cognitive deficits associated with Alzheimer's-disease-type pathologies.

Date: 2000
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DOI: 10.1038/35050103

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