Towards defining a rigidity-associated pathogenic pathway in idiopathic parkinsonism

R. John Dobbs*, Andre Charlett, Sylvia M. Dobbs, Clive Weller, Owens Iguodala, Cori Smee, James Bowthorpe, David Taylor, Ingvar T. Bjarnason

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)

Abstract

Helicobacter pylori eradication has a differential effect on the facets of idiopathic parkinsonism (IP): brady/hypokinesia improves, but rigidity worsens. Small intestinal bacterial overgrowth is common in IP and has been described as a sequel to Helicobacter eradication. The hyperhomocysteinaemia of IP is, in part, explained by serum vitamin B 12, but the concentration is not explained by Helicobacter status. Moreover, Helicobacter-associated gastric atrophy is uncommon in IP. However, overgrowth both increases B 12 utilization and provides a source of inflammation to drive homocysteine production. It is not a bystander event in IP: clouds of lysosomes are seen in duodenal enterocytes. Its candidature for causality of a rigidity-associated pathway is circumstantial: there are biological gradients of rigidity on natural killer and T-helper blood counts, both being higher with hydrogen breath test positivity for overgrowth.

Original languageEnglish
Pages (from-to)183-186
Number of pages4
JournalNeurodegenerative Diseases
Volume10
Issue number1-4
DOIs
Publication statusPublished - Apr 2012

Keywords

  • Aetiology/pathogenesis
  • Brady/hypokinesia
  • Helicobacter
  • Idiopathic parkinsonism
  • Natural killer lymphocytes
  • Rigidity
  • Small intestinal bacterial overgrowth
  • T-helper lymphocytes

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