Gut microbiota in ALS: possible role in pathogenesis?

ABSTRACT

Introduction: The gut microbiota has important roles in maintaining human health. The microbiota and its metabolic byproducts could play a role in the pathogenesis of neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS).

Areas covered: The authors evaluate the methods of assessing the gut microbiota, and also review how the gut microbiota affects the various physiological functions of the gut. The authors then consider how gut dysbiosis could theoretically affect the pathogenesis of ALS. They present the current evidence regarding the composition of the gut microbiota in ALS and in rodent models of ALS. Finally, the authors review therapies that could improve gut dysbiosis in the context of ALS.

Expert opinion: Currently reported studies suggest some instances of gut dysbiosis in ALS patients and mouse models; however, these studies are limited, and more information with well-controlled larger datasets is required to make a definitive judgment about the role of the gut microbiota in ALS pathogenesis. Overall this is an emerging field that is worthy of further investigation. The authors advocate for larger studies using modern metagenomic techniques to address the current knowledge gaps.

KEYWORDS:

• Amyotrophic lateral sclerosis
• neurodegeneration
• gut microbiota
• metagenomics
• dysbiosis
• microbiome

Article highlights

• The gut microbiota is important in human health

• With modern bio-informatics, the composition of the gut microbiota can be analyzed

• There are theoretical mechanisms by which abnormal gut microbiota could contribute to the pathogenesis of amyotrophic lateral sclerosis

• Some studies have found evidence of abnormality of altered gut microbiota in amyotrophic lateral sclerosis

• There is a need for further case-controlled studies

Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This paper was not funded