Intraneuronal beta-amyloid is a major risk factor - Novel evidence from the APP/PS1KI mouse model

2008 | conference paper. A publication with affiliation to the University of Göttingen.

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​Intraneuronal beta-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.​ (2008)
Neurodegenerative Diseases5(3-4) pp. 140​-142. ​8th International Conference on Alzheimers and Parkinsons Diseases​, Salzburg, AUSTRIA.
Basel​: Karger. DOI: https://doi.org/10.1159/000113684 

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Authors
Bayer, Thomas A.; Breyhan, Henning; Duan, Kailai; Rettig, Jens; Wirths, Oliver
Abstract
Accumulating evidence points to an important role of intraneuronal P-amyloid (AP) 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 A beta precursor protein and presenilin-1 knock-out (APP/PS1KI) mouse model with abundant intraneuronal A beta(42) 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 AP accumulation as a principal pathological trigger in AD. Copyright (c) 2008 S. Karger AG, Basel.
Issue Date
2008
Status
published
Publisher
Karger
Journal
Neurodegenerative Diseases 
Conference
8th International Conference on Alzheimers and Parkinsons Diseases
Conference Place
Salzburg, AUSTRIA
ISSN
1660-2854

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