Category: Parkinson's Disease: Pathophysiology
Objective: The association between excessive salt consumption, susceptibility to H. pylori infection and risk of Parkinson’s disease will be analyzed through scientific studies.
Background: The American Heart Association recommends adults should limit their salt (sodium chloride) intake to less than 2,300 milligrams daily; anything above this limit is classified as a “high-salt diet”(HSD) . Research shows excessive salt consumption stimulates the gastric mucosa, favoring Helicobacter pylori (H.pylori) colonization . It is proposed that those with HSD are inclined to H.pylori infection and consequently at risk of developing Parkinson’s disease (PD).
Method: A literature search was conducted across scientific, international databases for English, peer-reviewed articles and reviews published in the last decade using the following terms: Helicobacter pylori, high-salt diet, and Parkinson’s disease. Case reports were excluded. The main objectives were predominantly focused on animal-based studies.
Results: H.pylori releases bacterial factors that are toxic to neurons. Specifically, a PD toxin, chemically similar to that of methyl4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is found to induce damage to these cells . The changes made to gut microbiota by H.pylori infections results in systemic immune response, which crosses the gut-brain axis leading to neuroinflammation in the central nervous system . The infection is thought to spread via vagal innervation promoting the aggregation of α-synuclein. Studies have shown correlation between the expression of α-synuclein and the degree of inflammation caused by H.pylori gastritis . The chronic inflammatory reaction releases chemokines and inflammatory mediators which cross the blood brain barrier and leading to neuronal damage in the substantia nigra. Cytokines, IL-8, IL-1β, and TNF-α, have been found in microglia-mediated inflammation and neurotoxicity . Evidence shows cholesterol glucosides, which make up part of the lipid component of H. pylori aid, in the degeneration of neurons . The sterol glucosides cause loss of striatal dopaminergic terminals, an upregulation of the dopamine D2 receptor, causing reduced gait length and behavioral symptoms of PD.
Conclusion: Understanding the pathologic consequences of salt consumption on H.pylori is key in the prevention of PD. Further research is required for substantiation of causality, the role of antibiotics, and PD medication.
1]Cook, N. R., He, F. J., MacGregor, G. A., & Graudal, N. (2020). Sodium and health-concordance and controversy. BMJ (Clinical research ed.), 369, m2440. https://doi.org/10.1136/bmj.m2440
2]Gaddy, J. A., Radin, J. N., Loh, J. T., Zhang, F., Washington, M. K., Peek, R. M., Jr, Algood, H. M., & Cover, T. L. (2013). High dietary salt intake exacerbates Helicobacter pylori-induced gastric carcinogenesis. Infection and immunity, 81(6), 2258–2267. https://doi.org/10.1128/IAI.01271-12
3]McGee, D. J., Lu, X. H., & Disbrow, E. A. (2018). Stomaching the Possibility of a Pathogenic Role for Helicobacter pylori in Parkinson’s Disease. Journal of Parkinson’s disease, 8(3), 367–374. https://doi.org/10.3233/JPD-181327
4]Mossad, O., & Erny, D. (2020). The microbiota-microglia axis in central nervous system disorders. Brain pathology (Zurich, Switzerland), 30(6), 1159–1177. https://doi.org/10.1111/bpa.12908
5]Uberti, A. F., Callai-Silva, N., Grahl, M. V. C., Piovesan, A. R., Nachtigall, E. G., Furini, C. R. G., & Carlini, C. R. (2022). Helicobacter pylori Urease: Potential Contributions to Alzheimer’s Disease. International journal of molecular sciences, 23(6), 3091. https://doi.org/10.3390/ijms23063091
6]Schulz, J. D., Hawkes, E. L., & Shaw, C. A. (2006). Cycad toxins, Helicobacter pylori and parkinsonism: cholesterol glucosides as the common denomenator. Medical hypotheses, 66(6), 1222–1226. https://doi.org/10.1016/j.mehy.2004.12.033
7]Liu, H., Su, W., Li, S., Du, W., Ma, X., Jin, Y., Li, K., & Chen, H. (2017). Eradication of Helicobacter pylori infection might improve clinical status of patients with Parkinson’s disease, especially on bradykinesia. Clinical neurology and neurosurgery, 160, 101–104. https://doi.org/10.1016/j.clineuro.2017.07.003
To cite this abstract in AMA style:V. Balendra. Risk of Parkinson’s Disease due to Helicobacter Pylori and High Salt Consumption [abstract]. Mov Disord. 2023; 38 (suppl 1). https://www.mdsabstracts.org/abstract/risk-of-parkinsons-disease-due-to-helicobacter-pylori-and-high-salt-consumption/. Accessed September 23, 2023.
« Back to 2023 International Congress
MDS Abstracts - https://www.mdsabstracts.org/abstract/risk-of-parkinsons-disease-due-to-helicobacter-pylori-and-high-salt-consumption/