Amyotrophic lateral sclerosis as a protein level, non-genomic disease: Therapy with S2RM exosome released molecules

Abstract

Amyotrophic lateral sclerosis (ALS) is a rapidly progressing neurodegenerative disease that leads to death. No effective treatments are currently available. Based on data from epidemiological, etiological, laboratory, and clinical studies, I offer a new way of thinking about ALS and its treatment. This paper describes a host of extrinsic factors, including the exposome, that disrupt the extracellular matrix and protein function such that a spreading, prion-like disease leads to neurodegeneration in the motor tracts. A treatment regimen is described using the stem cell released molecules from a number of types of adult stem cells to provide tissue dependent molecules that restore homeostasis, including proteostasis, in the ALS patient. Because stem cells themselves as a therapeutic are cumbersome and expensive, and when implanted in a host cause aging of the host tissue and often fail to engraft or remain viable, only the S2RM molecules are used. Rebuilding of the extracellular matrix and repair of the dysfunctional proteins in the ALS patient ensues.

Keywords: Amyotrophic lateral sclerosis; Proteins; Stem cells; Extracellular matrix; Exposome; Heat shock protein; Stem cell molecules

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.