New Parkinson’s disease study
A big step forward in microbiome science
by Simon McGrath
New research on Parkinson’s disease, provides the best evidence yet that the gut microbiome can trigger inflammation in the brain, causing disease. Mady Hornig thinks a microbiome-brain link might play an important role in ME/CFS.
The new study, published in the prestigious journal Science, was done on mice. The mice were genetically engineered to develop Parkinson’s disease-like problems of movement and balance, as well as the molecular hallmarks of the disease. However, the researchers found that these mice didn’t develop symptoms if they were reared in a germ-free, sterile environment where they have no gut microbiome. Mice reared in normal, non-sterile conditions developed symptoms, but improved when treated with antibiotics (which kill off gut bacteria), again implicating a role for the microbiome.
And most intriguingly of all, transplanting gut microbes from Parkinson’s disease patients to these germ-free mice triggered symptoms of the disease. By contrast, germ-free mice receiving gut microbes from healthy humans did not develop symptoms, suggesting the gut bacteria in patients were playing a critical role in triggering problems.
The researchers also showed that the microbiome also triggered neuroinflammation with activation of microglia, the brain’s immune cells, alongside the symptoms. Several researchers have suggested that similar activation of microglia in ME/CFS patients could play a key role in our illness.
Finally, evidence in the paper indicates that the microbiome might be causing the symptoms and biological changes through releasing specific chemicals called small chain fatty acids. Bacteria produce these molecules when they break down dietary fiber. Feeding small chain fatty acids to germ-free mice (who lack a microbiome) triggered the Parkinson’s disease-like symptoms and the changes in the brain, though the researchers stressed that it’s likely other mechanisms are at play too.
It might be a coincidental finding, but Dr. Chris Armstrong has just published a small microbiome study that found elevated levels of small chain fatty acids in ME/CFS.
Although this study was only in a mouse model of Parkinson’s disease, it does provide good experimental evidence that the gut microbiome could play a key role in triggering the disease: both the symptoms and the underlying molecular pathology. That’s a big step forward in microbiome science.
Microbiome and disease: frontier science
Investigating the link between the microbiome and disease is frontier science right now. There are good reasons to suspect that the microbiome can trigger or perpetuate disease. They include the association of microbiome abnormalities with many diseases as well as clear potential mechanisms for such abnormalities to influence the brain and cause disease. But, it’s largely unexplored territory. This is the first clear experimental evidence the microbiome really could play a role in causing a brain disease – as opposed to just being simply the result of the disease.
It’s possible that a similar mechanism of gut microbiome changes affecting the brain could be at play in ME/CFS. Interestingly, the lead author of this new study, Professor Sarkis Mazmanian of CalTech, emphasized the implications of these findings beyond Parkinson’s disease, saying “we chose Parkinson’s as a model to test brain-gut interactions”.
As for the future, the CalTech team are trying to identify which bacteria might be most important in triggering Parkinson’s disease symptoms, either causing the symptoms or protecting against them. If they are successful, it could lead to new targeted microbiome therapies. This is the same goal that Mady Hornig and Ian Lipkin have for the Microbe Discovery Project if they find that the microbiome plays a critical role in ME/CFS for at least some patients.
The Microbe Discovery team gives a special thanks to Simon McGrath for this article