{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,1]],"date-time":"2026-11-01T03:57:20Z","timestamp":1793505440182,"version":"4.5.0"},"reference-count":66,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2019,1,17]],"date-time":"2019-01-17T00:00:00Z","timestamp":1547683200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["movementdisorders.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Movement Disorders"],"published-print":{"date-parts":[[2019,3]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Spread of \u03b1\u2010synuclein pathology from the peripheral to central nervous system may be an important etiological factor in Parkinson's disease, although there are some unanswered questions about its correlation with neuronal loss. Experimental evidence has highlighted the gastrointestinal tract as a potential starting point for aggregated \u03b1\u2010synuclein, with the vagus nerve acting as a \u201chighway\u201d by which pathology may be transmitted to the lower brain stem. This review begins by highlighting the key studies demonstrating that \u03b1\u2010synuclein pathology has the ability to spread from certain sites in the gastrointestinal tract to the brain (and vice versa). We go on to assess the recent epidemiological studies that have shown that vagotomy and appendectomy may have the potential to reduce the risk of developing Parkinson's disease. Finally, we discuss the factors in the gastrointestinal tract (such as dysbiosis of the gut microbiota, infection, and inflammation) that may trigger \u03b1\u2010synuclein aggregation in the first place, as well as other potential mechanisms underlying the distribution of \u03b1\u2010synuclein pathology in the brain. \u00a9 2019 International Parkinson and Movement Disorder Society<\/jats:p>","DOI":"10.1002\/mds.27556","type":"journal-article","created":{"date-parts":[[2019,1,17]],"date-time":"2019-01-17T11:55:25Z","timestamp":1547726125000},"page":"307-316","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":180,"title":["Gut\u2013brain axis and the spread of \u03b1\u2010synuclein pathology: Vagal highway or dead end?"],"prefix":"10.1002","volume":"34","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9643-3713","authenticated-orcid":false,"given":"David P.","family":"Breen","sequence":"first","affiliation":[{"name":"Centre for Clinical Brain Sciences University of Edinburgh  Edinburgh Scotland"},{"name":"Anne Rowling Regenerative Neurology Clinic University of Edinburgh  Edinburgh Scotland"},{"name":"Usher Institute of Population Health Sciences and Informatics University of Edinburgh  Edinburgh Scotland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0422-8398","authenticated-orcid":false,"given":"Glenda M.","family":"Halliday","sequence":"additional","affiliation":[{"name":"Brain and Mind Centre, Sydney Medical School University of Sydney  Camperdown Australia"},{"name":"School of Medical Sciences University of New South Wales  Kensington Australia"},{"name":"Neuroscience Research Australia  Randwick Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1229-3667","authenticated-orcid":false,"given":"Anthony E.","family":"Lang","sequence":"additional","affiliation":[{"name":"Edmond J. 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