Parkinson’s disease currently affects more than 6.1 million people worldwide. In addition to certain genetic and environmental factors involved in its etiology, recent work has suggested the possible role of an alteration of the intestinal microbiota (dysbiosis) in the triggering of the disease.
In rats, it has been demonstrated that protein aggregates, made up of the alpha-synuclein protein involved in Parkinson’s disease, can migrate from the intestine to the brainstem, via the vagus nerve. Studies also showed an increase in the abundance of certain bacteria in the microbiota of people with Parkinson’s disease, while other bacteria were reduced in quantity.
Dysbiosis can increase intestinal permeability and facilitate the passage of endotoxins from the intestine into the blood and to the brain where an inflammatory response would occur. Systemic and brain inflammation exacerbate alpha-synuclein aggregation and neuronal loss.
At the same time, it has been shown that European countries in which the prevalence of Parkinson’s disease has increased significantly over the past fifty years have consumed at least 6 times more broad-spectrum antibiotics than countries which have experienced a reduction in this prevalence. prevalence of this disease during the same period. This opens up the interesting, but little explored, avenue of a link between taking antimicrobials and the occurrence of Parkinson’s disease.
A new study has just been published on the subject. This is a nested case control study carried out in the United Kingdom, using NHS registers (National Health System). The authors compared data from more than 12,000 people with Parkinson’s disease with those from 80,000 controls. The objective was to analyze whether taking antimicrobials could have a link with the risk of Parkinson’s. Exposure to antimicrobials could have occurred between 1 and 15 years before the onset of illness.
The surprise comes from antifungals
The results are unexpected, and contrast with previous ones. The data indeed suggest an inverse and significant relationship between the number of penicillin treatments and the risk of Parkinson’s disease, regardless of the time since taking the antibiotic. For example, more than 5 treatments in the previous 1 to 5 years reduce the risk by 15%, in 6 to 10 years by 16%, in 11-15 years by 13%.
The relationship is also inverse but not significant between the number of treatments with macrolides or cephalosporins and the occurrence of the disease. The relationship between taking tetracyclines, lincosamide or imidazole could not be calculated.
On the other hand, more than 2 antifungal treatments prescribed within 1 to 5 years are associated with a 16% increase in the risk of Parkinson’s disease (OR 1.16; 95% CI 1.06 to 1.27). This result highlights the potential role of the intestinal mycobiome in Parkinson’s disease. A case-control study focusing on the mycobiome of patients with Parkinson’s disease highlighted differences with that of unaffected patients, and particularly designates Torulaspora delbrueckiivery common yeast.
The authors, however, moderate this observation: given the long latency period preceding the onset of Parkinson’s disease, the absence of a long-term association (> 10 years) leaves the possibility that exposure to antifungals is a marker, not a trigger for future disease. A case to follow…
