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A learning deficit related to age and beta-amyloid plaques in a mouse model of Alzheimer's disease.
Nature. 2000 Dec 21-28; 408(6815):975-9.Nat

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 beta-amyloid plaque formation that the hAPP mice display is puzzling. In the water maze, hAPP mice are impaired before and after amyloid plaque deposition. Here we show, using a new water-maze training protocol, that PDAPP mice also exhibit a separate age-related deficit in learning a series of spatial locations. This impairment correlates with beta-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 A beta overexpression and/or A beta 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.

Authors+Show Affiliations

Department of Neuroscience, University of Edinburgh, UK.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

11140684

Citation

Chen, G, et al. "A Learning Deficit Related to Age and Beta-amyloid Plaques in a Mouse Model of Alzheimer's Disease." Nature, vol. 408, no. 6815, 2000, pp. 975-9.
Chen G, Chen KS, Knox J, et al. A learning deficit related to age and beta-amyloid plaques in a mouse model of Alzheimer's disease. Nature. 2000;408(6815):975-9.
Chen, G., Chen, K. S., Knox, J., Inglis, J., Bernard, A., Martin, S. J., Justice, A., McConlogue, L., Games, D., Freedman, S. B., & Morris, R. G. (2000). A learning deficit related to age and beta-amyloid plaques in a mouse model of Alzheimer's disease. Nature, 408(6815), 975-9.
Chen G, et al. A Learning Deficit Related to Age and Beta-amyloid Plaques in a Mouse Model of Alzheimer's Disease. Nature. 2000 Dec 21-28;408(6815):975-9. PubMed PMID: 11140684.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - A learning deficit related to age and beta-amyloid plaques in a mouse model of Alzheimer's disease. AU - Chen,G, AU - Chen,K S, AU - Knox,J, AU - Inglis,J, AU - Bernard,A, AU - Martin,S J, AU - Justice,A, AU - McConlogue,L, AU - Games,D, AU - Freedman,S B, AU - Morris,R G, PY - 2001/1/5/pubmed PY - 2001/2/28/medline PY - 2001/1/5/entrez SP - 975 EP - 9 JF - Nature JO - Nature VL - 408 IS - 6815 N2 - 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 beta-amyloid plaque formation that the hAPP mice display is puzzling. In the water maze, hAPP mice are impaired before and after amyloid plaque deposition. Here we show, using a new water-maze training protocol, that PDAPP mice also exhibit a separate age-related deficit in learning a series of spatial locations. This impairment correlates with beta-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 A beta overexpression and/or A beta 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. SN - 0028-0836 UR - https://www.unboundmedicine.com/medline/citation/11140684/A_learning_deficit_related_to_age_and_beta_amyloid_plaques_in_a_mouse_model_of_Alzheimer's_disease_ L2 - https://doi.org/10.1038/35050103 DB - PRIME DP - Unbound Medicine ER -