miR126-5p Downregulation Facilitates Axon Degeneration and NMJ Disruption via a Non-Cell-Autonomous Mechanism in ALS.

Authors

Roy Maimon, Tel Aviv University
Ariel Ionescu, Tel Aviv University
Avichai Bonnie, Tel Aviv University
Sahar Sweetat, Hebrew University of Jerusalem
Shane Wald-Altman, Tel Aviv University
Shani Inbar, Tel Aviv University
Tal Gradus, Tel Aviv University
Davide Trotti, Thomas Jefferson UniversityFollow
Miguel Weil, Tel Aviv University
Oded Behar, Hebrew University of Jerusalem
Eran Perlson, Tel Aviv University

Document Type

Article

Publication Date

6-13-2018

Comments

This article has been peer reviewed. It is the author’s final published version in Journal of Neuroscience, Volume 38, Issue 24, June 2018, Pages 5478-5494.

The published version is available at https://doi.org/10.1523/JNEUROSCI.3037-17.2018. Copyright © Maimon et al.

Abstract

Axon degeneration and disruption of neuromuscular junctions (NMJs) are key events in amyotrophic lateral sclerosis (ALS) pathology. Although the disease's etiology is not fully understood, it is thought to involve a non-cell-autonomous mechanism and alterations in RNA metabolism. Here, we identified reduced levels of miR126-5p in presymptomatic ALS male mice models, and an increase in its targets: axon destabilizing Type 3 Semaphorins and their coreceptor Neuropilins. Using compartmentalized

Recommended Citation

Maimon, Roy; Ionescu, Ariel; Bonnie, Avichai; Sweetat, Sahar; Wald-Altman, Shane; Inbar, Shani; Gradus, Tal; Trotti, Davide; Weil, Miguel; Behar, Oded; and Perlson, Eran, "miR126-5p Downregulation Facilitates Axon Degeneration and NMJ Disruption via a Non-Cell-Autonomous Mechanism in ALS." (2018). Farber Institute for Neuroscience Faculty Papers. Paper 31.
https://jdc.jefferson.edu/farberneursofp/31

Creative Commons License

This work is licensed under a Creative Commons Attribution 4.0 License.

PubMed ID

29773756

Language

English