Gut microbes, blood metabolites may be Huntington’s biomarkers
Levels can distinguish people with, without disease, study finds
Examining the amounts of certain microbes in the gut and levels of specific metabolites in the blood may help distinguish people with and without Huntington’s disease with 100% accuracy, a study suggested.
“This study determined crucial functional gut microbiota and potential biomarkers associated with [Huntington’s development], providing new insights into the role of the gut microbiota-brain axis in [Huntington’s] occurrence and development,” the researchers wrote.
The study, “Multi-omics Analysis Reveals Key Gut Microbiota and Metabolites Closely Associated with Huntington’s Disease,” was published in Molecular Neurobiology.
Huntington’s is an inherited neurodegenerative disorder caused by defects in the HTT gene, resulting in a range of symptoms that include movement, cognitive, and psychiatric problems.
Gut microbiota refers to the collection of microorganisms that reside in the gastrointestinal tract. These microbes play important roles in various aspects of human health, including communicating with the nervous system via the so-called gut-brain axis. Metabolites generated by gut microbes are important molecules that can influence multiple functions in the human body.
Types of microbes differ in patients
Emerging evidence suggests that people with Huntington’s have dysbiosis, or an altered gut microbiota. Whether their metabolic profiles are also altered, however, remains unclear.
To know more, researchers in China collected fecal and blood samples from Huntington’s patients and healthy individuals to investigate their gut microbiomes and metabolites and identify potential disease biomarkers.
Fecal samples were subjected to genetic analysis to identify the different types of microbes, and blood samples were tested for the presence of metabolites.
While no differences were found between patients and controls in the diversity and richness of gut microbes within individual fecal samples, the abundance of certain types of microbes was altered.
At the genus level, which refers to groups of closely related bacterial species, some microbes were more abundant in Huntington’s patients. These included Bacteroides, Faecalibacterium, Parabacteroides, Alistipes, Dialister, and Christensenella.
At the same time, some groups of bacteria, such as Lachnospira, Roseburia, Clostridium, Ruminococcus, Blautia, Butyricicoccus, Agathobaculum, Phocaeicola, Coprococcus, and Fusicatenibacter, were less abundant in patients.
Blood tests also showed that samples from patients could easily be distinguished from those of controls based on metabolite levels. Of the 244 metabolites found at different levels in patients than controls, 107 metabolites were at higher levels, and 137 were at lower levels.
Nearly half (40.1%) of the metabolites that differed were fat molecules called lipids and lipid-like molecules. Many of these metabolites were significantly involved in various metabolic pathways of certain carbohydrates, lipids, nucleotides, or DNA and RNA components.
The team identified several metabolites that distinguished between people with and without Huntington’s with high accuracy. These included dimethisterone at 91.1% accuracy, propylparaben at 91.5%, vanillin at 97.9%, tulipinolide at 100%, p-hydroxymandelic acid at 99.7%, and esculetin at 97.6%.
However, when data from the top 30 significantly different metabolites and the top 30 gut microbiota were combined, the accuracy rose to 100%. In comparison, the accuracy using just gut microbiota data was 86.3%.
“Our research provides direct evidence for the role of the gut microbiota dysregulation and the brain-gut axis in [Huntington’s],” the authors wrote. “In the future, well-designed longitudinal studies with a larger sample size, accounting for confounding variables are required.”
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