Bacteria and Parkinson's Disease
Although they are invisible to the naked eye, trillions of bacteria call our bodies home. It has been estimated that 38 trillion (38,000,000,000,000) bacteria live on the skin, or in the mouth, intestines and urinary tract of each human being. The composition of bacteria in and on the body is referred to as the microbiota. Many things determine the nature of an individual’s microbiota: 1) whether birth was vaginal or by Caesarean section; 2) whether infant nutrition was by breastmilk or formula; 3) race and ethnic background; and 4) diet, environment, occupation and medications. Bacterial populations are critical to human health, contributing to nutrition, metabolism and immune function. New techniques that identify bacteria by their genetic material led to the current state of knowledge in which up to 99% of the human microbiota have been identified.
While it makes sense that the makeup of the intestinal bacterial population may be important in the development of intestinal diseases, a new body of evidence suggests that changes in intestinal bacteria may also be important in disorders as diverse as obesity, cardiac and vascular disease, and neurological illnesses, including PD.
There are now nine published research studies that suggest changes in the bacterial populations in the intestines of people with Parkinson's. The studies are performed by analysis of bacterial genes in stool samples. Each of these studies has shown differences in stool bacteria between research subjects with PD and healthy control subjects. Some early studies of animals with experimental “PD” produced by toxins or genetic engineering show that populating the animal intestines with PD stool increased the severity of the toxic or genetic animal “PD.” However none of the microbiota studies to date points to a specific bacterial culprit. Rather it appears that the bacteria living in the PD intestines share properties that lead to increased inflammation in the intestinal wall and in the body as a whole. Inflammation in the body may be an important determinant of PD onset or progression.
One of the most important limitations to these studies is that it is impossible to say yet whether these changes in bacteria might be important drivers of the disease process or whether they simply are a result of the disease. This “chicken and egg” argument remains unresolved. We know that brain cell degeneration begins to occur years before PD can be diagnosed, and it will be important to discover whether microbiota changes occur in this prodromal period as well. Moreover, intensive animal experimentation may help us better understand the links between microbiota changes and inflammation and the true role of inflammation in disease genesis and progression.
Should changes in microbiota prove important in disease origin or progression, these studies will help to illuminate new treatment strategies for PD.
Kathleen M. Shannon, MD presented at the First World Parkinson Congress in Washington DC and the Fourth World Parkinson Congress in Portland, OR. She currently serves as Detling Professor and Chair for the Department of Neurology at the University of Wisconsin School of Medicine and Public Health.
Ideas and opinions expressed in this post reflect that of the author(s) solely. They do not necessarily reflect the opinions of the World Parkinson Coalition®