Impaired synaptic plasticity and learning in aged amyloid precursor protein transgenic mice

Chapman, P. F., White, G. L., Cooper-Blacketer, D., Marshall, V. J., Irozarry, M., Younkin, L., Good, Mark Andrew ORCID: https://orcid.org/0000-0002-1824-1203, Bliss, T. V. P., Hyman, B. T., Younkin, S. G. and Hsaio, K. K. 1999. Impaired synaptic plasticity and learning in aged amyloid precursor protein transgenic mice. Nature Neuroscience 2 (3) , pp. 271-276. 10.1038/6374

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Abstract

We investigated synaptic communication and plasticity in hippocampal slices from mice overexpressing mutated 695-amino-acid human amyloid precursor protein (APP695SWE), which show behavioral and histopathological abnormalities simulating Alzheimer's disease. Although aged APP transgenic mice exhibit normal fast synaptic transmission and short term plasticity, they are severely impaired in in-vitro and in-vivo long-term potentiation (LTP) in both the CA1 and dentate gyrus regions of the hippocampus. The LTP deficit was correlated with impaired performance in a spatial working memory task in aged transgenics. These deficits are accompanied by minimal or no loss of presynaptic or postsynaptic elementary structural elements in the hippocampus, suggesting that impairments in functional synaptic plasticity may underlie some of the cognitive deficits in these mice and, possibly, in Alzheimer's patients.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Psychology
Subjects:	B Philosophy. Psychology. Religion > BF Psychology R Medicine > RC Internal medicine > RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry
Publisher:	Nature Publishing Group
ISSN:	1097-6256
Last Modified:	21 Oct 2022 09:00
URI:	https://orca.cardiff.ac.uk/id/eprint/35037

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