Over recent years, researchers have become increasingly interested in the link between the immune system and Parkinson’s disease. Using a mouse model, scientists recently explored the potential role of a bacterial gut infection. Share on Pinterest A recent study examines how a gut infection might trigger Parkinson’s disease. Parkinson’s disease develops due to the slow depletion of dopamine-producing neurons in a part of the brain called the substantia nigra. This region of the brain plays an important role in movement, so symptoms include shaking, tremor, and rigidity. The primary risk factor for Parkinson’s is age and, as the population of the United States is slowly aging, the number of cases is steadily growing. Some believe that we are approaching a Parkinson’s pandemic; globally, between 1990–2015, the number of Parkinson’s cases has doubled to more than 6 million. Some predict the number to double again to 12 million by 2040. Although researchers have studied the disease for decades, they still have many questions about how and why brain cells are destroyed.

Parkinson’s and the immune system More recently, links between the immune system and Parkinson’s have come to the fore. Evidence is slowly mounting that Parkinson’s might have an autoimmune component. Autoimmune diseases are conditions where an individual’s immune system confuses the body’s cells for pathogens and destroys them. A recent study, published in Nature, tests this theory further; the researchers hail from the Université de Montréal, the Montreal Neurological Institute, and McGill University, all in Canada. Around 10 percent of Parkinson’s cases are due to mutations in genes that code for the proteins PINK1 and Parkin, which play a role in clearing out damaged mitochondria. Individuals who carry these mutations are more likely to develop Parkinson’s at an earlier age — before the age of 50. However, when scientists knock these genes out of mice, the mice do not develop Parkinson’s disease or any similar symptoms. Why these knock-out mice are immune to Parkinson’s has foxed researchers. According to the authors, it means that “factors other than the loss of function of these proteins are likely to be required to trigger Parkinson’s.” They set out to identify these other factors.

Joining the dots The authors wanted to find further evidence that there is a link between PINK1 and Parkin proteins, mitochondria, the immune system, and Parkinson’s. They believe that knock-out mice do not develop Parkinson’s because of how the researchers have reared them. The mice used in these studies are typically germ-free, meaning that they have never encountered bacteria. So, to test this hypothesis, they infected young mice that lacked PINK1 and Parkin with Escherichia coli. This caused mild intestinal symptoms in the mice. As expected, the early-life infection triggered the occurrence of Parkinson’s-like motor symptoms as they got older. The scientists also identified a loss of dopaminergic neurons in their brains. When the scientists gave the mice L-DOPA — a drug used to treat the symptoms of Parkinson’s — their symptoms improved, inferring that the condition has similarities to the human condition. In mice with normal versions of PINK1 and Parkin, the immune system deals with pathogens appropriately. However, the authors believe that in animals without the Parkinson’s-related genes, the gut infection triggers an abnormal immune response that overruns and attacks healthy cells.