One study showed that the presence of antibodies to H. pylori was associated with poorer stride length, which improved following its eradication. As duodenum is the primary site for levodopa absorption, it is postulated that H. pylori infection BAY-60-7550 affects levodopa bioavailability by disrupting the duodenal mucosa, and producing reactive oxygen species, which could inactivate the drug. We found that as high as 32.9% of our PD patients tested positive for H. pylori infection. This is consistent with findings from a previous case-control study conducted in our center involving a different cohort of PD patients, which yielded a prevalence of 48%. On the other hand, studies in patients with other neurological conditions such as epilepsy failed to consistently demonstrate an association with H. pylori infection. Despite extensive research in this area, it remains unclear why PD patients have higher propensity to develop this infection. In addition to the high prevalence, this study showed that H. pylori infection affected patients’ motor performances adversely, most likely by interfering with levodopa action. We showed that even at baseline, the H. pylori-positive patients had much poorer motor scores based on the total UPDRS and subsections I-IV, compared to H. pylori-negative patients, despite being matched for duration and stage. From as early as 6 weeks of eradication therapy, there was a significant overall improvement in the motor severity scores by approximately 15%, which was sustained and in fact improved further over the subsequent 6 weeks by 25%. Paralleling the clinical motor improvement, patients also reported significant improvement in their quality of life, for most of the domains tested, particularly ADL which improved by 22%. These quality of life improvements were also observed from as early as 6 weeks. As this study did not have a placebo arm, we were unable to determine to what extent the observed improvement could have been contributed by a placebo effect or the expectation of reward, mediated by striatal dopamine release. Nevertheless, a previous randomized placebo-controlled double-blind study involving a small number of PD patients showed that H. pylori eradication improved clinical symptoms and plasma levodopa levels, compared to the placebo group which received only antioxidants. The authors concluded that this improvement was due better levodopa absorption post eradication. In correlating the motor and ADL improvements to levodopa action, we found that eradication of H.pylori significantly improved both the levodopa onset time by approximately 14 minutes at week 12 post eradication, and the duration of ON by approximately 56 minutes at 6 weeks, and 38 minutes at 12 weeks post eradication. Hence, as suggested previously, the clinical improvement following H. pylori eradication was most probably due to better levodopa absorption in the gut, which translated to an improvement in clinical fluctuations.