Eradicating Helicobacter pylori Infections May Be a Key Treatment for Parkinson’s Disease

A study published in the Journal of Parkinson’s Disease suggests that Helicobacter pylori may play a role in Parkinson’s disease (PD) as well.

While human genetic mutations are involved in a small number of PD cases, the vast majority of cases are of unknown environmental causes, prompting enormous interest in identifying environmental risk factors involved.

David J. McGee, PhD, LSU Health Sciences Center-Shreveport, Shreveport, Louisiana, and colleagues conducted a literature review to explore the association between H pylori and PD. They uncovered 4 key findings:
● People with PD were 1.5 to 3 times more likely to be infected with H pylori than people without PD.
● Patients with PD and H pylori displayed worse motor functions than patients with PD who did not have H pylori.
● Eradication of H pylori improved motor function in patients with PD compared with patients whose infection was not eradicated.
● Eradication of H pylori improved levodopa absorption in patients compared with those whose infection was not eradicated.

“This is an in-depth and comprehensive review that summarises all the major papers in the medical literature on Parkinson’s disease and H pylori,” said Dr. McGee. “Our conclusion is that there is a strong enough link between the H pylori and Parkinson’s disease that additional studies are warranted to determine the possible causal relationship.”

The investigators also analysed existing studies to try and find possible testable pathways between the bacterial infection and Parkinson’s to lay the groundwork for future research. They found 4 main possible explanations for the association: (1) bacterial toxins produced by H pylori may damage neurons; (2) the infection triggers a massive inflammatory response that causes damage to the brain; (3) H pylori may disrupt the normal gut microbial flora; and (4) the bacteria might interfere with the absorption properties of levodopa.

The onset of PD is often preceded by gastrointestinal dysfunction, suggesting that the condition might originate in the gut and spread to the brain along the brain-gut axis.

Screening patients with PD for the presence of H pylori and subsequent treatment if positive with triple drug therapy may contribute to improved levodopa absorption and ultimately improve symptoms of PD.

“Evidence for a strong association among H pylori chronic infection, peptic ulceration, and exacerbation of PD symptoms is accumulating,” said Dr. McGee. “However, the hypotheses that H pylori infection is a predisposing factor, disease progression modifier, or even a direct cause of PD remain largely unexplored. This gut pathology may be multifactorial, involving H pylori, intestinal microflora, inflammation, misfolding of alpha-synuclein in the gut and brain, cholesterol and other metabolites, and potential neurotoxins from bacteria or dietary sources. Eradication of H pylori or return of the gut microflora to the proper balance in PD patients may ameliorate gut symptoms, L-dopa malabsorption, and motor dysfunction.”


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