Gut Microbiota Regulate Motor Deficits and Neuroinflammation in a Model of Parkinson?s Disease
Timothy R. SampsonPress enter key for correspondence informationPress enter key to Email the author
, Justine W. Debelius
, Taren Thron
, Stefan Janssen
, Gauri G. Shastri
, Zehra Esra Ilhan
, Collin Challis
, Catherine E. Schretter
, Sandra Rocha
, Viviana Gradinaru
, Marie-Francoise Chesselet
, Ali Keshavarzian
, Kathleen M. Shannon9
, Rosa Krajmalnik-Brown
, Pernilla Wittung-Stafshede
, Rob Knight
, Sarkis K. Mazmanian10,Press enter key for correspondence informationPress enter key to Email the author
9Present address: Department of Neurology, University of Wisconsin-Madison, Madison, WI 53705, USA
10Lead Contact
DOI: http://dx.doi.org/10.1016/j.cell.2016.11.018
Our findings establish that the microbiota are required for the hallmark motor and GI dysfunction in a mouse model of PD, via postnatal gut-brain signaling by microbial molecules that impact neuroinflammation and αSyn aggregation. Coupled with emerging research that has linked gut bacteria to disorders such as anxiety, depression, and autism, we propose the provocative hypothesis that certain neurologic conditions that have classically been studied as disorders of the brain may also have etiologies in the gut.
DOI: http://dx.doi.org/10.1016/j.cell.2016.11.018
Timothy R. SampsonPress enter key for correspondence informationPress enter key to Email the author
, Justine W. Debelius
, Taren Thron
, Stefan Janssen
, Gauri G. Shastri
, Zehra Esra Ilhan
, Collin Challis
, Catherine E. Schretter
, Sandra Rocha
, Viviana Gradinaru
, Marie-Francoise Chesselet
, Ali Keshavarzian
, Kathleen M. Shannon9
, Rosa Krajmalnik-Brown
, Pernilla Wittung-Stafshede
, Rob Knight
, Sarkis K. Mazmanian10,Press enter key for correspondence informationPress enter key to Email the author
9Present address: Department of Neurology, University of Wisconsin-Madison, Madison, WI 53705, USA
10Lead Contact
DOI: http://dx.doi.org/10.1016/j.cell.2016.11.018
Our findings establish that the microbiota are required for the hallmark motor and GI dysfunction in a mouse model of PD, via postnatal gut-brain signaling by microbial molecules that impact neuroinflammation and αSyn aggregation. Coupled with emerging research that has linked gut bacteria to disorders such as anxiety, depression, and autism, we propose the provocative hypothesis that certain neurologic conditions that have classically been studied as disorders of the brain may also have etiologies in the gut.
DOI: http://dx.doi.org/10.1016/j.cell.2016.11.018