Compositional and functional alterations of gut microbiota in patients with stroke.

BACKGROUND AND AIMS: There is accumulating evidence that gut microbiota plays a key role in cardiovascular diseases. Gut bacteria can transform dietary choline, l-carnitine, and trimethylamine N-oxide (TMAO) into trimethylamine, which can be oxidized into TMAO again in the liver. However, the alterations of the gut microbiota in large artery atherosclerotic (LAA) stroke and cardioembolic (CE) stroke have been less studied. METHODS AND RESULTS: We performed a case-control study in patients with LAA and CE types of strokes. We profiled the gut microbiome using Illumina sequencing of the 16S ribosomal RNA gene (V4-V5 regions), and TMAO was determined via liquid chromatography-tandem mass spectrometry. Our results showed that the TMAO levels in the plasma of patients with LAA and CE strokes were significantly higher than those in controls (LAA stroke, 2931 ± 456.4 ng/mL; CE stroke, 4220 ± 577.6 ng/mL; healthy control, 1663 ± 117.8 ng/mL; adjusted p < 0.05). The TMAO level in the plasma of patients with LAA stroke was positively correlated with the carotid plaque area (rho = 0.333, 95% CI = 0.08-0.55, p = 0.0093). Notably, the composition and the function of gut microbiota in the LAA stroke group were significantly different from those in the control group (FDR-adjusted p-value < 0.05). There was no significant association between gut microbiota and CE stroke in our study. CONCLUSION: This study provides evidence for significant compositional and functional alterations of the gut microbiome in patients with LAA stroke. Gut microbiota might serve as a potential biomarker for patients with LAA stroke.

Serum levels of chromogranins and secretogranins correlate with the progress and severity of Parkinson's disease.

Little is known about the relevance of chromogranins (Cgs) and secretogranins (Sgs) in Parkinson's disease (PD). In this study, we determined serum levels of CgA, CgB, and SgII in PD patients and assessed their association with disease severity. PD patients were recruited, identified, and classified as having early (n = 14), intermediate (n = 18), or late (n = 4) stage disease according to Hoehn-Yahr scores. The serum concentrations of CgA, CgB, and SgII in patients with well-defined PD (n = 36) and in healthy controls (n = 52) were measured by enzyme-linked immunosorbent assay. Compared with controls, serum CgA levels were significantly elevated and serum SgII levels were significantly reduced in PD patients (both P < 0.05). There was no difference in serum CgB levels between the two groups. Both serum CgA and SgII levels changed progressively over time from early to intermediate to late stage (P < 0.05). Spearman correlation analysis revealed that serum CgA and SgII levels correlated with Hoehn-Yahr and UPDRS scores (P < 0.001). These results indicate that changes in serum levels of CgA and SgII may be closely related to the severity of PD.