Suspect bacterium may trigger Parkinson’s

Mouse study finds stomach ulcer-causing microbes may also affect brain

NEW ORLEANS — Brain cells may be the latest victim of a bacterial bad guy already charged with causing ulcers and stomach cancer.

Helicobacter pylori, a bacterium that lives in the stomachs of about half the people in the world, may help trigger Parkinson’s disease, researchers reported May 22 at a meeting of the American Society for Microbiology. Parkinson’s disease is a neurological disorder that kills dopamine-producing cells in some parts of the brain. People with the disease have trouble controlling their movements. About 60,000 new cases of the disease are diagnosed each year in the United States.

Some previous studies have suggested that people with Parkinson’s disease are more likely than healthy people to have had ulcers at some point in their lives and are more likely to be infected with H. pylori. But until now those connections between the bacterium and the disease have amounted to circumstantial evidence.

Now researchers are gathering evidence that may pin at least some blame for Parkinson’s disease on the notorious bacterium.

Middle-aged mice infected with the ulcer-causing bacterium developed abnormal movement patterns over several months of infection, said Traci Testerman, a microbiologist at Louisiana State University Health Sciences Center in Shreveport. Young mice infected with the bacterium didn’t show any signs of movement problems. Testerman’s colleague, neuroscientist Michael Salvatore, found that Helicobacter-infected mice make less dopamine in parts of the brain that control movement, possibly indicating that dopamine-making cells are dying just as they do in Parkinson’s disease patients.

The bacteria didn’t have to be alive to cause the problem. Feeding mice killed H. pylori produced the same effect, suggesting that some biochemical component of the bacterium is responsible.

A candidate for the disease-causing molecule is modified cholesterol. Helicobacter can’t make its own cholesterol, so it steals cholesterol from its host and then sticks a sugar molecule on it. The structure of the modified cholesterol resembles a toxin from a tropical cycad; people in Guam who have eaten the plant’s seeds have developed a disease called ALS-parkinsonism dementia complex. Testerman and her colleagues are trying to determine if the modified cholesterol alone can lead to Parkinson-like symptoms in mice or if some other factor from the bacterium is also needed.

Even if the scientists show that H. pylori can cause or contribute to Parkinson’s disease, it’s not clear whether getting rid of the organism would be a good thing. Although the bacterium causes ulcers and stomach cancer, it also helps protect against allergies, asthma and esophageal cancer and other acid reflux diseases. It is hard to know at this point exactly how letting Helicobacter stay or making it go will affect any individual person, said microbiologist Stanley Maloy of San Diego State University. But it is clear that a possible link between Parkinson’s disease and the stomach bacterium can no longer be ignored.

“There’s enough solid data that it would be wrong not to look into it more closely,” Maloy said.

Tina Hesman Saey is the senior staff writer and reports on molecular biology. She has a Ph.D. in molecular genetics from Washington University in St. Louis and a master’s degree in science journalism from Boston University.

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