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Updated: Jul 20, 2026

ALS - Motor Neuron Disease: Mechanism and Development of New Therapies
Published on: July 29, 2007
Hypothesis: a motor neuron toxin produced by a clostridial species residing in gut causes ALS
W T Longstreth1, J S Meschke, S K Davidson
1Department of Neurology, School of Medicine, University of Washington, Seattle, Washington, USA. wl@u.washington.edu
Abstract:
We hypothesize that a yet-to-be-identified motor neuron toxin produced by a clostridial species causes sporadic amyotrophic lateral sclerosis (ALS) in susceptible individuals. This clostridial species would reside undetected in the gut and chronically produce a toxin that targets the motor system, like the tetanus and botulinum toxins. After gaining access to the lower motor neuron, the toxin would be transported back to the cell body, as occurs with the tetanus toxin, and destroy the lower motor neuron - the essential feature of ALS. Again like the tetanus toxin, some of the toxin would cross to neighboring cells and to the upper motor neuron and similarly destroy these motor neurons. Weakness would relentlessly progress until not enough motor neurons remained to sustain life. If this hypothesis were correct, treatment with appropriate antibiotics or antitoxins might slow or halt progression of disease, and immunization might prevent disease.
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