Gut Microbiomes in HD

Status Not yet recruiting

Clinical Trial Summary

The purpose of this study is to find out if there is a connection between the naturally occurring bacteria in our bodies and the progression of Huntington disease. The investigators are trying to determine if patients who are diagnosed with adult-onset HD and who exhibit a rapid rate of disease progression have unique populations of bacteria in their gut as compared to patients with slower progression.

Clinical Trial Description

Two of the most common non-neurological features of Huntington disease (HD) are progressive weight loss and metabolic dysfunction. However, a small proportion of HD patients are pathologically overweight, despite having similar CAG repeat lengths as pathologically underweight patients. The investigators hypothesize this spectrum of weight abnormalities may be caused by HD-related metabolic dysfunction. Pathological weight loss is recapitulated in transgenic HD model mice expressing fragments of human huntingtin (HTT), either transgenically3,4 or knocked-in to a portion of the mouse HD homolog (Hdh) gene5. Conversely, pathological weight gain is recapitulated in transgenic HD model mice expressing full-length human HTT either along with the full complement of Hdh6,7 or in Hdh-null backgrounds8,9. In Hdh-null background transgenic HD model mice, which are pathologically overweight, circadian feeding is disrupted, despite maintenance of naturally nocturnal circadian activity. Interestingly, circadian feeding patterns are restored by suppression of brain HTT (unpublished Dr. Amber Southwell), suggesting that HTT plays a role in circadian feeding regulation. Furthermore, when circadian feeding patterns are artificially restored with scheduled feeding, striatal HTT is temporarily suppressed, while metabolic markers and body weight are normalized (unpublished Dr. Amber Southwell). Together, this demonstrates that HTT is involved in gut-brain feedback, but since HTT suppression during scheduled feedings is transient, while metabolic effects are lasting, HTT is likely not the master regulator of this feedback loop. Instead, the gut microbiome may influence this pathway, possibly contributing to the onset and/or progression of HD. ;

Study Design

Related Conditions & MeSH terms

Huntington Disease

Clinical Trial Details

NCT number	NCT06448546
Study type	Observational
Source	University of Central Florida
Contact	Amoy Fraser, PhD, CCRP, PMP
Phone	4072668742
Email	amoy.fraser@ucf.edu
Status	Not yet recruiting
Phase
Start date	June 2024
Completion date	June 2029

View Details

See also
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Clinical trials are conducted in a series of steps, called phases - each phase is designed to answer a separate research question.

Phase 1: Researchers test a new drug or treatment in a small group of people for the first time to evaluate its safety, determine a safe dosage range, and identify side effects.
Phase 2: The drug or treatment is given to a larger group of people to see if it is effective and to further evaluate its safety.
Phase 3: The drug or treatment is given to large groups of people to confirm its effectiveness, monitor side effects, compare it to commonly used treatments, and collect information that will allow the drug or treatment to be used safely.
Phase 4: Studies are done after the drug or treatment has been marketed to gather information on the drug's effect in various populations and any side effects associated with long-term use.