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

Creative Commons License

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

PubMed ID

29773756

Language

English

Available for download on Thursday, December 13, 2018

Included in

Neurosciences Commons

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