A common bacteria that infects the human stomach has significant links with worsened symptoms of Parkinson’s disease, researchers have found.
Researchers at the University of Malaya analysed a small group of Parkinson’s disease patients with and without a common infection of the stomach lining caused by the bacterium Helicobacter pylori. Their results showed that those with the infection, around a third of the total, tested worse in motor problems related to Parkinson’s disease.
Parkinson’s disease is the world’s second most common neurodegenerative disorder, causing tremors and decreasing motor coordination. Causes are elusive and doctors currently can only treat its symptoms.
Patients whose infection could be treated and eradicated showed fewer Parkinson’s disease symptoms in motor performance tests, while those who stayed infected had further declines in their test results.
Over 50% of the world’s population carries H. pylori, with the highest infection rates in Asian countries. It affects mucous membranes in the gut and causes chronic infections, often contracted during childhood.
H. pylori can cause a range of digestive tract disorders and can linger indefinitely unless treated, although some subjects show few symptoms.
The researchers have proposed two main theories to explain their results. The first is that the infection may reduce the uptake of levodopa, a drug that reduces symptoms of Parkinson’s disease.
More speculatively, chronic H. pylori infections might aggravate or even trigger Parkinson’s disease. However, they also speculate that it’s possible that Parkinson’s disease may make subjects more prone to contracting the infection.
The researchers say their limited study of 103 subjects aimed mainly to confirm the link between Helicobacter pylori infection and Parkinson’s disease suggested by previous, less rigorous research. In addition to its size, the study was limited by the fact that it took place in a single Malaysian clinic and that it was cross-sectional; so it was essentially a data snapshot taken at a certain place and time.
But they say the link they found between the infection and worsened symptoms of Parkinson’s disease is strong enough to justify further, larger, well-designed clinical trials to confirm it and investigate its causes in more depth.
Development of Parkinson’s Disease
A similar 2011 study from Traci Testerman of Louisiana State University Health Sciences Center found that H. pylori could play a role in the development of Parkinson’s disease.
“Infection of late middle-aged mice with a particular strain of the bacteria Helicobacter pylori results in development of Parkinson’s disease symptoms after 3-5 months,” says Testerman, who presented the research. “Our findings suggest that H. pylori infection could play a signficant role in the development of Parkinson’s disease in humans.”
In fact, physicians have noted a correlation between stomach ulcers and Parkinson’s disease as far back as the 1960s, before it was even known that H. pylori was the cause of ulcers.
More recently, a number of studies found that people with Parkinson’s disease were more likely to be infected with the bacterium, and that Parkinson’s patients who were treated and cured of infection showed slight improvement compared to controls that continued to deteriorate.
Testerman and her colleagues developed an animal model to more effectively understand the role of H. pylori and its modified cholesterol in Parkinson’s disease.
They infected young and aged mice with three different strains of the bacteria and monitored their locomotor activity and dopamine levels in the brain. Mice infected with one of the strains showed significant reductions in both.
“The results were far more dramatic in aged mice than in young mice, demonstrating that normal aging increases susceptibility to Parkinsonian changes in mice, as is seen in humans,” says Testerman.
In Guam, a study of why some populations had a high risk of developing a Parkinson’s-like disease discovered that a specific compound in cycad seeds eaten by these populations was neurotoxic. The compound, which resembles a cholesterol with an attached sugar group, is almost identical to a compound produced by H. pylori.