For roughly 15 years, it has been hypothesized that Parkinson’s disease does not originate exclusively in the brain, but also in the intestines. However, the potential biological mechanisms involved remain to be elucidated.
Parkinson’s disease affects 6.3 million people worldwide1, the majority over 50 years old. It is caused by neuron loss in the substantia nigra, which controls movement. Motor symptoms gradually develop, such as slowness of movement, muscle rigidity and tremors, but also sleeping disturbances, depressive episodes and gastrointestinal disorders2.
The primary risk factor is age, but genetic predisposition3 and environmental causes, like exposure to pesticides4, have also been identified. A hypothesis has been germinating over the past 15 years about a potential role of the intestinal microbiota in the development of the disease.
An emerging hypothesis
The idea was originally advanced after observing a connection between chronic infection with Helicobacter pylori bacteria and the risk of developing Parkinson’s disease5. Dysbiosis was also observed more frequently in Parkinson’s disease patients, notably with fewer supposedly “anti-inflammatory” bacteria and more “pro-inflammatory” bacteria6. However, a cause-and-effect relationship between abnormal intestinal microbiota and Parkinson’s disease has not yet been demonstrated.
A therapeutic hope
Currently, management focuses on limiting motor symptoms of the disease with dopamine precursors or, more rarely, deep brain stimulation7. But those treatments do not prevent disease progression. Therefore, acting very early on the microbiota through nutritional or pharmacological interventions, to lower the risk of developing the disease by correcting dysbiosis, is an option currently being considered8 .
1- Dorsey ER et al. Projected number of people with Parkinson disease in the most populous nations, 2005 through 2030. Neurology. 2007;68(5):384–386. https://www.ncbi.nlm.nih.gov/pubmed/17082464
2- Clairembault T et al. Structural alterations of the intestinal epithelial barrier in Parkinson’s disease. Acta Neuropathol Commun 2015a; 3:12. https://actaneurocomms.biomedcentral.com/articles/10.1186/s40478-015-0196-0
3- Cheon SM et al. Genetics of Parkinson's disease—a clinical perspective. J Mov Disord. 2012; 5(2):33–41. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4027661/pdf/jmd-5-2-33-1.pdf
4- Elbaz A et al. Professional exposure to pesticides and Parkinson’s disease. Ann Neurol 2009; 66 (4): 494-504. http://onlinelibrary.wiley.com/wol1/doi/10.1002/ana.21717/full
5- Dobbs SM et al. Link between Helicobacter pylori infection and idiopathic parkinsonism. Med Hypotheses. 2000;55:93–8. https://www.ncbi.nlm.nih.gov/pubmed/10904422
6- Keshavarzian A et al. Colonic bacterial composition in Parkinson’s disease. Mov Disord 2015; 30: 1351-60. http://onlinelibrary.wiley.com/doi/10.1002/mds.26307/abstract
7- Bronstein J et al. . (2011). Deep brain stimulation for Parkinson disease: an expert consensus and review of key issues. Arch. Neurol. 68, 165. 10.1001/archneurol.2010.260 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4523130/pdf/nihms691775.pdf
8- Mulak A, Bonaz B. Brain-gut-microbiota axis in Parkinson's disease. World J Gastroenterol. 2015;21:10609-20. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4588083/pdf/WJG-21-10609.pdf