Gut microbiome changes linked to progress of Huntington's disease

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Gut microbiome changes have already been described in neurological diseases and conditions like Alzheimer's and Parkinson's, autism and depression, among others. ©Getty Images

Australian scientists have made a rare breakthrough in the study of Huntington's disease by finding that changes in the gut microbiome may influence its progress and treatment.

The research points to the urgent need for follow-up studies in humans that can validate the findings. It provides even more evidence that the gut plays a significant role in diseases of the brain.

Gut microbiome changes have already been described in Alzheimer’s and Parkinson’s disease, autism, depression, chronic fatigue syndrome, type 2 diabetes and other diseases.

Huntington’s disease is a fatal degenerative disease inherited from a parent, in which brain cells begin to die leading to onset of symptoms in a person’s mid-30s to 40s, and sometimes earlier, with 5% of sufferers having juvenile onset.

Dysfunctional and dying brain cells cause gradually worsening movement symptoms, dementia and eventually death. Huntington’s patients can also suffer from psychiatric symptoms, including depression.

Anthony Hannan, a world-renowned authority on the disease processes underlying Huntington’s, was the first to show that environmental enrichment can slow down the inexorable decline.

Now Professor Hannan and colleagues the Florey Institute of Neuroscience and Mental Health in Melbourne have probed the relative levels of gut bacteria in mice, and found dramatic differences between healthy mice and genetically engineered mice that will develop Huntington’s as they age.

Bacterial differences

The study, published in the journal Neurobiology of Disease, showed that male Huntington’s disease mice had different proportions of various bacteria compared to their healthy siblings. Intriguingly, they also ate more food but gained weight at a lower rate.

As their guts became dysfunctional and excreted excess water in faecal matter, the first movement symptoms of the disease would appear. However, the researchers are unable to say at this stage whether the altered microbiome plays any role in the timing of symptom onset.

Researchers are excited about the possibility that understanding the link between the microbiome and disease could lead to new therapeutic approaches,” said Professor Hannan.

Before we jump that hurdle, though, we really need to know whether these same changes are seen in Huntington’s patients. I strongly suspect they will be, as this is a very accurate model of the disease. Furthermore, the bacteria that live in the gut of mice are similar to those in the human gut, therefore such microbiome studies have direct clinical relevance.”

Over 2500 Australians are diagnosed with Huntington’s at any one time - approximately the same frequency as other neurodegenerative diseases like motor neurone disease. Huntington’s is caused by a mutated copy (a ‘genetic stutter’) of the Huntington gene.

Family members who inherit the gene mutation will always get the disease, and have a 50 per cent chance of passing it on to their children. Huntington’s research is chronically under-funded and therefore under-studied.