Gut Bacteria Sugars Identified as Potential Trigger for ALS and Frontotemporal Dementia

Researchers discover that inflammatory glycogen from gut bacteria triggers brain damage in ALS and FTD, opening the door for gut-targeted treatments.

By: AXL Media

Published: Apr 26, 2026, 8:30 AM EDT

Source: Information for this report was sourced from ScienceAlert

The Gut-Brain Connection in Neurodegeneration

A new study has revealed that bacterial sugars produced in the gut may be a hidden contributor to Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal Dementia (FTD). These two conditions are closely linked, involving the progressive death of neurons that control muscle movement, behavior, and language. Led by Case Western Reserve University, the research team found that certain harmful gut bacteria produce inflammatory forms of glycogen that trigger an overactive immune response, ultimately damaging the brain and breaking down the blood-brain barrier.

The Role of the C9ORF72 Gene

The research focused on the C9ORF72 gene, a common genetic variant linked to both ALS and FTD. While many people carry this variant, not all develop the diseases, leading scientists to search for environmental "second triggers." Using engineered mouse models, the team discovered that the protein normally produced by the C9ORF72 gene acts as a "brake" on inflammatory glycogen. When this gene is mutated or absent, the body loses its ability to regulate these bacterial sugars, allowing the inflammatory chain reaction to proceed unchecked.

Identifying the Bacterial Culprit

Through methodical testing of various microbiome mixes, the researchers identified Parabacteroides merdae as a primary strain responsible for producing the harmful glycogen. When introduced to mice, this specific bacteria caused significant brain inflammation. Crucially, the team validated these findings in humans; stool samples from ALS and FTD patients showed significantly higher levels of inflammatory glycogen compared to healthy controls. This suggests that the presence of these microbes may be a critical environmental factor in disease onset.