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Molecules 2018, 23(4), 718; https://doi.org/10.3390/molecules23040718

Synaptic Alterations in Mouse Models for Alzheimer Disease—A Special Focus on N-Truncated Abeta 4-42

1
Division of Molecular Psychiatry, Department of Psychiatry and Psychotherapy, University Medical Center (UMG), Georg-August-University, von-Siebold-Strasse 5, 37075 Göttingen, Germany
2
Center for Nanoscale Microscopy and Molecular Physiology of the Brain (CNMPB), Humboldtallee 23, 37073 Göttingen, Germany
3
Center for Physiology and Pathophysiology, Institute for Neuro- and Sense Physiology, University Medical Center (UMG), Georg-August-University, Humboldtallee 23, 37073 Göttingen, Germany
*
Author to whom correspondence should be addressed.
Academic Editors: Birgit Hutter-Paier and Stephan Schilling
Received: 21 February 2018 / Revised: 16 March 2018 / Accepted: 19 March 2018 / Published: 21 March 2018
(This article belongs to the Special Issue 25th Anniversary of the Amyloid Hypothesis and Alzheimer Disease)
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Abstract

This commentary reviews the role of the Alzheimer amyloid peptide Aβ on basal synaptic transmission, synaptic short-term plasticity, as well as short- and long-term potentiation in transgenic mice, with a special focus on N-terminal truncated Aβ4-42. Aβ4-42 is highly abundant in the brain of Alzheimer’s disease (AD) patients. It demonstrates increased neurotoxicity compared to full length Aβ, suggesting an important role in the pathogenesis of AD. Transgenic Tg4-42 mice, a model for sporadic AD, express human Aβ4-42 in Cornu Ammonis (CA1) neurons, and develop age-dependent hippocampal neuron loss and neurological deficits. In contrast to other transgenic AD mouse models, the Tg4-42 model exhibits synaptic hyperexcitability, altered synaptic short-term plasticity with no alterations in short- and long-term potentiation. The outcomes of this study are discussed in comparison with controversial results from other AD mouse models. View Full-Text
Keywords: Alzheimer’s disease; N-truncated Aβ; transgenic mouse models; long-term potentiation; electrophysiology; synapse; field potential; Tg4-42 Alzheimer’s disease; N-truncated Aβ; transgenic mouse models; long-term potentiation; electrophysiology; synapse; field potential; Tg4-42
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).
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Dietrich, K.; Bouter, Y.; Müller, M.; Bayer, T.A. Synaptic Alterations in Mouse Models for Alzheimer Disease—A Special Focus on N-Truncated Abeta 4-42. Molecules 2018, 23, 718.

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