Therapeutics Advances
Copyright ©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Stem Cells. Nov 26, 2017; 9(11): 187-202
Published online Nov 26, 2017. doi: 10.4252/wjsc.v9.i11.187
Amyotrophic lateral sclerosis as a protein level, non-genomic disease: Therapy with S2RM exosome released molecules
Greg Maguire
Greg Maguire, BioRegenerative Sciences, Inc., La Jolla, CA 92037, United States
Author contributions: Maguire G wrote the artcle.
Conflict-of-interest statement: Maguire G is owner of BioRegenerative Sciences.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Dr. Greg Maguire, BioRegenerative Sciences, Inc., 505 Coast Blvd., La Jolla, CA 92037, United States. gmaguire@bioregenerativesciences.com
Telephone: +1-858-5219203
Received: May 29, 2017
Peer-review started: June 1, 2017
First decision: July 17, 2017
Revised: August 23, 2017
Accepted: September 3, 2017
Article in press: September 3, 2017
Published online: November 26, 2017
Core Tip

Core tip: The author propose that amyotrophic lateral sclerosis is a disease of damaged and misfolded proteins induced by environmental regulators, occurring at the level of translation and post-translation, and not at the level of the genome. The damaged proteins disrupt the extracellular matrix surrounding neurons, precluding normal communication between neurons and the neural stem cells that surround the neurons. As a consequence, the neural stem cells no longer properly shuttle heat shock proteins to the neurons, and many proteins within the neuron misfold. The misfolded proteins are prion-like, leading to a spreading, destructive sequelae within and between neurons and other cells in the nervous system.