by https://www.nature.com/articles/s41531-024-00724-z
Summary and speculative perspectives of the current study are indicated in Fig. 7. In this study, we showed that fecal biosyntheses of riboflavin and biotin were decreased in PD, which were accounted for by different bacteria in two groups of countries. We also showed that decreased fecal biosyntheses of riboflavin and biotin were correlated with decreased fecal polyamines and SCFAs. The following speculations emerge from our findings and previous studies. Decreased SCFAs and polyamines lead to thinning of the mucus layers47, which increases the intestinal permeability. Indeed, the intestinal permeability was increased in PD5,48. Increased intestinal permeability may expose the intestinal nerve plexus to pesticides, herbicides, and other toxins49, and lead to abnormal aggregation of α-synuclein fibrils. In addition, SCFAs and polyamines facilitate M2 macrophage polarization and relatively decreases M1 macrophage50, and their deficiency induces neuroinflammation51. We thus hypothesize that gut dysbiosis in PD causes decreased fecal productions of SCFAs and polyamines, which enhances intestinal α-synuclein fibril formation and neuroinflammation.
