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Proof\u2010of\u2010principle that infection can contribute to IP was provided by case studies and a placebo\u2010controlled efficacy study of <jats:italic>Helicobacter <\/jats:italic> eradication. \u201cMalignant\u201d IP appears converted to \u201cbenign\u201d, but marked deterioration accompanies failure. Similar benefit on brady\/hypokinesia from eradicating \u201clow\u2010density\u201d infection favors autoimmunity. Although a minority of UK probands are urea breath test positive for <jats:italic>Helicobacter<\/jats:italic>, the predicted probability of having the parkinsonian label depends on the serum <jats:italic>H. pylori <\/jats:italic>antibody profile, with clinically relevant gradients between this \u201cdiscriminant index\u201d and disease burden and progression. In IP, <jats:italic>H. pylori <\/jats:italic>antibodies discriminate for persistently abnormal bowel function, and specific abnormal duodenal enterocyte mitochondrial morphology is described in relation to <jats:italic>H. pylori<\/jats:italic> infection. Slow intestinal transit manifests as constipation from the prodrome. Diarrhea may flag secondary small\u2010intestinal bacterial overgrowth. This, coupled with genetically determined intense inflammatory response, might explain evolution from brady\/hypokinetic to rigidity\u2010predominant parkinsonism.<\/jats:p>","DOI":"10.1111\/j.1523-5378.2008.00622.x","type":"journal-article","created":{"date-parts":[[2008,8,13]],"date-time":"2008-08-13T04:57:57Z","timestamp":1218603477000},"page":"309-322","source":"Crossref","is-referenced-by-count":49,"title":["<i>Helicobacter<\/i> Hypothesis for Idiopathic Parkinsonism: Before and Beyond"],"prefix":"10.1111","volume":"13","author":[{"given":"R. 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