| First Author | Sampson TR | Year | 2016 |
| Journal | Cell | Volume | 167 |
| Issue | 6 | Pages | 1469-1480.e12 |
| PubMed ID | 27912057 | Mgi Jnum | J:238066 |
| Mgi Id | MGI:5818071 | Doi | 10.1016/j.cell.2016.11.018 |
| Citation | Sampson TR, et al. (2016) Gut Microbiota Regulate Motor Deficits and Neuroinflammation in a Model of Parkinson's Disease. Cell 167(6):1469-1480.e12 |
| abstractText | The intestinal microbiota influence neurodevelopment, modulate behavior, and contribute to neurological disorders. However, a functional link between gut bacteria and neurodegenerative diseases remains unexplored. Synucleinopathies are characterized by aggregation of the protein alpha-synuclein (alphaSyn), often resulting in motor dysfunction as exemplified by Parkinson's disease (PD). Using mice that overexpress alphaSyn, we report herein that gut microbiota are required for motor deficits, microglia activation, and alphaSyn pathology. Antibiotic treatment ameliorates, while microbial re-colonization promotes, pathophysiology in adult animals, suggesting that postnatal signaling between the gut and the brain modulates disease. Indeed, oral administration of specific microbial metabolites to germ-free mice promotes neuroinflammation and motor symptoms. Remarkably, colonization of alphaSyn-overexpressing mice with microbiota from PD-affected patients enhances physical impairments compared to microbiota transplants from healthy human donors. These findings reveal that gut bacteria regulate movement disorders in mice and suggest that alterations in the human microbiome represent a risk factor for PD. |
