Synaptic alterations in mouse models for Alzheimer disease—A special focus on N-truncated abeta 4-42

19Citations
Citations of this article
33Readers
Mendeley users who have this article in their library.

Abstract

This commentary reviews the role of the Alzheimer amyloid peptide Aß 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 Aß4-42. Aß4-42 is highly abundant in the brain of Alzheimer’s disease (AD) patients. It demonstrates increased neurotoxicity compared to full length Aß, suggesting an important role in the pathogenesis of AD. Transgenic Tg4-42 mice, a model for sporadic AD, express human Aß4-42 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.

Cite

CITATION STYLE

APA

Dietrich, K., Bouter, Y., M ller, M., & Bayer, T. A. (2018). Synaptic alterations in mouse models for Alzheimer disease—A special focus on N-truncated abeta 4-42. Molecules. MDPI AG. https://doi.org/10.3390/molecules23040718

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free