Mice show symptoms matching those of humans with Parkinson's disease when exposed to the gut bacteria of Parkinson's patients, and got better when treated with antibiotics. If the discovery is found to apply to humans, it will open up new and potentially easier paths to treating the world's second most common neurodegenerative disease.

The last few years have seen an astonishingly rapid growth in the number of conditions suspected of being related to bacteria inhabiting the gut. Asthma, multiple sclerosis, and depression are just three of many recent examples.

The possibility that Parkinson's disease should be added to the list was raised by the observation that gastrointestinal symptoms not only often accompany the disease, but appear before more recognized signs. Three studies published last year all showed differences between the bacteria in the guts of people with Parkinson's disease and others of the same age.

Professor Sarkis Mazmanian of the California Institute of Technology noted that little had been done to test if the intestinal symptoms triggered Parkinson's or were just an early warning sign. He turned to a previously developed line of genetically modified mice with a condition considered similar enough to Parkinson's to be used as a research model.

Mazmanian raised some of these mice in sterile cages to ensure they were kept free from harmful bacteria, while others were kept in more normal conditions. Those exposed to fewer germs performed much better at a range of tasks, such as climbing poles and removing adhesive from their noses, in some cases almost matching mice without the Parkinson's-like genetics. Moreover, autopsies revealed fewer of the misfolded proteins associated with Parkinson's disease in the mice kept in clean cages.

Even where mice had been raised with exposure to bacteria, antibiotics reduced their symptoms, Mazmanian revealed in Cell.

Perhaps most suggestively of all, the low-symptom mice got much sicker when given fecal transplants from Parkinson's patients than when given transplants from healthy humans. It is important to note, however, that only mice with a genetic predisposition to Parkinson's-like symptoms responded in this way. Other mice were unaffected by the fecal transplants.

The details of the way gut bacteria could affect dopamine-releasing cells, whose malfunction causes Parkinson's, remain uncertain. However, the paper notes that we already know that gut bacteria can influence immune cells in the brain, and there are multiple paths by which changes to these immune cells could trigger Parkinson's disease.

Although Parkinson's disease has a genetic component, fewer than 10 percent of cases are considered hereditary, indicating that environmental effects dominate, yet we know very little about the triggers, let alone the mechanisms, for this.

An aging population, combined with the fact that 1 percent of people over 60 have Parkinson's, has brought a wealth of research attention to the disease, but new treatments have not kept pace. If Mazmanian's findings extend to humans, it may prove much easier to alter the gut microbiome than to protect damaged neurons from what ails them.

“There are some reports of antibiotics (and even bowel cleansing, which removes bacteria) leading to temporary improvements in motor functions," Mazmanian told IFLScience. "But these are single cases, not controlled, and thus anecdotal without larger clinical studies. I am not sure of any epidemiological data linking increased antibiotic use throughout one’s lifetime to protection from Parkinson's disease.”

The antibiotics given to the mice killed beneficial bacteria as well, and the authors stress treatment will only be possible after we can identify which strains of bacteria are to blame.