Amyotrophic lateral sclerosis (ALS), also called Lou Gehrig’s disease, is a fatal neuromuscular disorder characterized by progressive loss of motor neurons and severe skeletal muscle atrophy. Currently, there is no cure for ALS. Most patients die within 5 years after disease onset. The lifetime risk of ALS is about 1 in 472 in women and 1 in 350 in men . Treatment with the only US FDA approved drug, Riluzole, extends patient life span only for a few months with little improvement in ALS symptoms . Thus, there is an urgent need to further understand the pathogenic mechanisms in order to develop novel interventions for alleviating disease progression and improving the quality of life for ALS patients. Although the massive decline of the neuromuscular system is the most overwhelming phenomenon in ALS, other organs may also actively contribute to the progressive loss of neuromuscular function in the disease progression. In a recently published study on an ALS mouse model, for the first time we noticed that changes in intestinal function occurred in young ALS mice before the disease onset, indicating a possibility that altered intestinal homeostasis takes place along the decline of neuromuscular function in ALS. We reasoned that an impaired gut-neuromuscular crosstalk may actively contribute to ALS progression. This editorial article discusses a potential contribution of gut defects in the course of ALS.
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