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Vol. 5, No. 3-4, 2008
Issue release date: March 2008
Neurodegenerative Dis 2008;5:140–142
(DOI:10.1159/000113684)

Intraneuronal β-Amyloid Is a Major Risk Factor – Novel Evidence from the APP/PS1KI Mouse Model

Bayer T.A. · Breyhan H. · Duan K. · Rettig J. · Wirths O.
aDepartment of Psychiatry, Division of Molecular Psychiatry, University of Goettingen, Goettingen, and bInstitute of Physiology, Saarland University, Homburg, Germany

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Abstract

Accumulating evidence points to an important role of intraneuronal β-amyloid (Aβ) in the development of Alzheimer’s disease (AD), with its typical clinical symptoms like memory impairment and changes in personality. We have previously reported on the Aβ precursor protein and presenilin-1 knock-out (APP/PS1KI) mouse model with abundant intraneuronal Aβ42 accumulation and a 50% loss of CA1 neurons at 10 months of age. In addition, we observed reduced short- and long-term synaptic plasticity, hippocampal neuron loss, and reduced performance in a working memory task. These observations support a pivotal role of intraneuronal Aβ accumulation as a principal pathological trigger in AD.



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