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dc.contributor.authorChen, Guiquan
dc.contributor.authorChen, Karen S
dc.contributor.authorKnox, Jane H
dc.contributor.authorInglis, Jennifer
dc.contributor.authorBernard, Andrew
dc.contributor.authorMartin, Stephen J
dc.contributor.authorJustice, Alan
dc.contributor.authorMcConlogue, Lisa
dc.contributor.authorGames, Dora
dc.contributor.authorFreedman, Stephen B
dc.contributor.authorMorris, Richard G M
dc.coverage.spatial5en
dc.date.accessioned2005-02-16T16:18:33Z
dc.date.available2005-02-16T16:18:33Z
dc.date.issued2000-12-21
dc.identifier.citationChen GQ, Chen KS, Knox J, Inglis J, Bernard A, Martin SJ, Justice A, McConlogue L, Games D, Freedman SB, Morris RGM, NATURE, 408 (6815): 975-979 DEC 21 2000en
dc.identifier.urihttp://www.nature.com/
dc.identifier.urihttp://hdl.handle.net/1842/708
dc.description.abstractMice 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 b-amyloid plaque formation that the hAPP mice display is puzzling. In the water maze (1), hAPP mice are impaired before and after amyloid plaque deposition (2-7). Here we show, using a new watermaze training protocol, that PDAPP mice (8) also exhibit a separate age-related deficit in learning a series of spatial locations. This impairment correlates with b-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 Ab overexpression and/or Ab 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.en
dc.format.extent5479 bytes
dc.format.mimetypetext/plain
dc.language.isoen
dc.publisherNature Publishing Groupen
dc.subjectpathologyen
dc.subjectb-amyloiden
dc.subjectalzheimers diseaseen
dc.titleA learning deficit related to age and b-amyloid plaques in a mouse model of Alzheimer's diseaseen
dc.typeArticleen


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