Towards defining a rigidity-associated pathogenic pathway in idiopathic parkinsonism.
| Autor: | Dobbs RJ; Institute of Pharmaceutical Sciences, King's College London, London, UK., Charlett A, Dobbs SM, Weller C, Iguodala O, Smee C, Bowthorpe J, Taylor D, Bjarnason IT |
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| Jazyk: | angličtina |
| Zdroj: | Neuro-degenerative diseases [Neurodegener Dis] 2012; Vol. 10 (1-4), pp. 183-6. Date of Electronic Publication: 2011 Dec 23. |
| DOI: | 10.1159/000332807 |
| Abstrakt: | 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. (Copyright © 2011 S. Karger AG, Basel.) |
| Databáze: | MEDLINE |
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