Does Glyphosate Acting as a Glycine Analogue Contribute To ALS?
Wendy A. Morley2, Michael J. Hadden3, Martin C. Michener4
Affiliation
- 1Computer Science and Artificial Intelligence Laboratory, MIT, Cambridge MA 02139 USA
- 2Thionetic Nutrition, Richmond Hill, ON L4C 957 Canada
- 3CTE-HOPE, Indianola, IA 50125 USA
- 4School of Landscape Architecture, Boston Architectural College, Newbury St. Boston MA 02115 USA
Corresponding Author
Stephanie Seneff, Computer Science and Artificial Intelligence Laboratory, MIT, Cambridge, MA 02139, USA, E-mail: seneff@csail.mit.edu
Citation
Seneff, S., et al. Does glyphosate acting as a glycine analogue contribute to ALS? (2017) Bioinfo Proteom Img Anal 2(2): 140- 160.
Copy rights
© 2017 Seneff, S. This is an Open access article distributed under the terms of Creative Commons Attribution 4.0 International License.
Keywords
Abstract
Amyotrophic Lateral Sclerosis (ALS) is a fatal neurodegenerative disease involving several protein mutations in glycine-rich regions with limited treatment options. 90 - 95% of all cases are non-familial with epidemiological studies showing a significant increased risk in glyphosate-exposed workers. In this paper, we propose that glyphosate, the active ingredient in Roundup®, plays a role in ALS, mainly through mistakenly substituting for glycine during protein synthesis, disruption of mineral homeostasis as well as setting up a state of dysbiosis. Mouse models of ALS reveal a pre-symptomatic profile of gut dysbiosis. This dysbiotic state initiate a cascade of events initially impairing metabolism in the gut, and, ultimately, through a series of intermediate stages, leading to motor neuron axonal damage seen in ALS. Lipopolysaccharide, a toxic by-product of dysbiosis which contributes to the pathology, is shown to be statistically higher in ALS patients. In this paper we paint a compelling view of how glyphosate exerts its deleterious effects, including mitochondrial stress and oxidative damage through glycine substitution. Furthermore, its mineral chelation properties disrupt manganese, copper and zinc balance, and it induces glutamate toxicity in the synapse, which results in a die-back phenomenon in axons of motor neurons supplying the damaged skeletal muscles.