Progress and Prospects in Parkinson's Research/Causes/Infection/Helicobacter pylorii

For decades medical science attributed the onset of stomach ulcers to a diet containing spicy food, or too much stomach acid or to stress. In this last instance the vagus nerve was postulated as a likely channel for infection between the CNS and the digestive system.

In 1979 a Medical Registrar named Barry Marshall teamed up with Robin Warren a pathologist at the Royal Perth Hospital, Australia and developed and published the hypothesis that bacterial infection and in particular colonies of helicobacter pylori, (HP)embedded in the lining of the duodenum, were responsible for the appearance of stomach ulcers, This was greeted with scepticism by the medical establishment on the grounds that such bacteria could not survive in a solution of stomach acid. This argument was strengthened when Marshall and Warren failed to reproduce the condition in pigs in 1984.

At this point Marshall decided to prove the theory by drinking the contents of a Petri dish infected with Helicobacter pylori. He thought it might take a year for an ulcer to develop, but went on to develop acute gastric inflammation within days.. One of the early symptoms was halitosis from the waste products given off by bacteria. Also he failed to produce antibodies hinting that some people may have a natural genetic immunity to HP. He was awarded the Nobel prize for physiology in 2005.

Now, in a complete reversal of the theory that nervous stress is responsible for gastric malfunction, some researchers are postulating that this bacterium may be the trigger for PD.

Background edit

Helicobacter_pylori is a bacterium, which takes up residence in the human digestive system. Some estimates put the proportion of people infected at 50%. Some 80% of infected people experience no symptoms and there is some speculation that it might have a beneficial effect. But for others it has been associated with the onset of chronic gastritis, duodenal ulcers and stomach cancer. It is treatable with regular antibiotics.

Research edit


Strang [1] evaluated the relationship between stomach ulcers and the onset of PD.

A cohort was formed of 250 randomly selected PD patients over 35 and a control group of a near relative without PD. 23 PD patients had confirmed duodenal ulceration compared with 9 in the control group. The average time interval between the onset of ulcer and PD symptoms was 18 years for males and 10 years for females.


Szabo et al [2] demonstrated that dosing rats with the PD-inducing drug MPTP also resulted in ther development of duodenal ulcers.

The ulcers were prevented by pretreatment with dopamine agonists (e.g., bromocriptine, lergotrile) or monoamine oxidase inhibitors (e.g., pargyline, 1-deprenyl).

High doses of MPTP also caused gastric erosions and motility changes resembling parkinsonism (e.g., akinesia, rigidity, forward bending of trunk). This chemical decreased gastric secretion of acid and pepsin, as well as pancreatic bicarbonate, trypsin and amylase.

Thus, MPTP causes duodenal ulcers that are possibly associated with impaired defence in the duodenal bulb.


Altschuler, E. [3] (1996)was the first person to publish the hypothesis that Helicobacter might be a causaive agent for PD.


Dobbs et al [4] examined PD patients with low Body Mass Index and Helicobacter infection. When these last two factors were corrected in one patient, a reversal of PD symptoms was observed.

Bjarnason et al [5] measured the effect of Helicobacter eradication on a cohort of PD patients. Their conclusions were:-

Interim analysis points to a direct or surrogate (not necessarily unique) role of a particular infection in the pathogenesis of parkinsonism. With eradication failure, bolus release of antigen from killed bacteria could aggravate an effect of ongoing infection.

Weller et al [6] assessed whether the presence of Heilcobacter antibodies in blood serum could serve as a biomarker for PD. Their conclusions:-

The apparent importance of H. pylori in the etiology/pathogenesis of idiopathic parkinsonism is not confined to those with evidence of current infection.


Dobbs et al [7] pt forward the hypothesis that Helicobacter infection might be a causative agent for PD.


Tan, and Goh[8] reviewed the evidence for helicobacter infection being responsible for diseases outside of the digestive system.

Nielsen et al [9] tested the hypothesis that infection with Helicobacter pylori (HP) contributes to the development of Parkinson's disease (PD.

Data was collected for 4484 patients with a first time PD diagnosis between 2001 and 2008 from the Danish National Patient Register (DNPR) and 22, 416 population controls from the Danish Civil Registration System (CRS) together with information on drug use from the National Prescription Registry (NPR).

Population-based study suggests that chronic HP infections and/or gastritis contribute to PD or that these are PD-related pathologies that precede motor symptoms.

Further Reading edit


Kountouras, J.; Zavos, C.; Polyzos, S.A.; Deretzi, G.; Vardaka, E.; Giartza-Taxidou, E.; Katsinelos, P.; Rapti, E.; Chatzopoulos, D.; Tzilves, D.; Stergiopoulos, C. and Christodoulou, K. AbstractEur J Neurol. 2012 Jun;19(6):e56 Helicobacter pylori infection and Parkinson's disease: apoptosis as an underlying common contributor.

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Related Pages edit

References edit


  1. Strang, R. R. (1965) Abstract Med. J. Austr. 52 842 – 843 The Association of gastro-duodenal ulceration with Parkinson’s disease
  2. Szabo, S.; Brown, A.; Pihan,; G.; Dali, H. and Neumeyer, J.L. (1979) Abstract Proc. Soc Exp. Biol. Med.180 (3):567-571.Duodenal ulcer induced by MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine).
  3. Altschuler, E. Hypotheses. 47 (5):413 – 414 . Gastric Helicobacter pylori infection as a cause of idiopathic Parkinson disease and non-arteric anterior optic ischemic neuropathy.
  4. Dobbs ,R.J.; Dobbs, S.M.; Weller, C.; Bjarnason, I.T.; Oxlade, N.L.; Charlett, A.; Al-Janabi, M.A.; Kerwin, R.W.; Mahler, R.F. and Price, A.B. (2005) Abstract Helicobacter 10(4):267- 275. Role of chronic infection and inflammation in the gastrointestinal tract in the etiology and pathogenesis of idiopathic parkinsonism. Part 1: eradication of Helicobacter in the cachexia of idiopathic parkinsonism.
  5. Bjarnason, I.T.; Charlett, A.; Dobbs, R.J.; Dobbs, S.M.; Ibrahim, M.A.; Kerwin, R.W.; Mahler, R.F.; Oxlade, N.L.; Peterson, D.W.; Plant, J.M.; Price, A.B. and Weller, C. (2005) Abstract Helicobacter. 10(4):276-287. Role of chronic infection and inflammation in the gastrointestinal tract in the etiology and pathogenesis of idiopathic parkinsonism. Part 2: response of facets of clinical idiopathic parkinsonism to Helicobacter pylori eradication. A randomized, double-blind, placebo-controlled efficacy study.
  6. Weller, C.; Charlett, A.; Oxlade, N.L.; Dobbs, S.M.; Dobbs, R.J.; Peterson, D.W. and Bjarnason, I.T.(2005) Abstract Helicobacter. 10(4):288-297. Role of chronic infection and inflammation in the gastrointestinal tract in the etiology and pathogenesis of idiopathic parkinsonism. Part 3: predicted probability and gradients of severity of idiopathic parkinsonism based on H. pylori antibody profile.
  7. Dobbs, R.J.; Dobbs, S.M.; Weller, C.; Charlett, A.; Bjarnason, I.T.; Curry, A.; Ellis, D.S.; Ibrahim, M.A.; McCrossan, M.V.; O'Donohue, J.; Owen, R.J., Oxlade, N.L.; Price, A.B.; Sanderson, J.D.; Sudhanva, M. and Williams, J. (2008) Abstract Helicobacter. 13 (5):309-22. Helicobacter hypothesis for idiopathic parkinsonism: before and beyond.
  8. Tan, H.J. and Goh, K.L. (2012) Abstract J. Dig. Dis.13(7):342-9 Extragastrointestinal manifestations of Helicobacter pylori infection: Facts or myth? A critical review.
  9. Nielsen, H.H.; Qiu, J.; Friis,S. Wermuth, L. and Ritz, B. (2012)Abstract Eur. J. Neurol. (6):864-869 Treatment for Helicobacter pylori infection and risk of Parkinson's disease in Denmark.