1,7-Dimethyluric acid, a metabolite of caffeine, was elevated in the control and PD-/LRRK2+ groups compared with the PD+/LRRK2+ group. Although this metabolite was not found in the dust, the parent compound (caffeine) was identified, without significant differences but with an average higher normalized peak intensity in the control group (Figure ). These results agree with previous studies , , which proposed lower levels of caffeine and caffeine metabolites as potential diagnostic biomarkers for early PD. Caffeine, a common psychostimulant, has shown neuroprotective effects (via reduction of Reactive Oxygen Species (ROS)) and appears to improve motor symptoms in PD , . Lower levels of caffeine and its metabolites in PD patients might be explained by a malabsoption in the small intestine. Although microbiome dysbiosis is a common feature in PD, to date it remains unclear whether caffeine malabsorption in PD is influenced by this .