{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,26]],"date-time":"2026-06-26T11:30:27Z","timestamp":1782473427741,"version":"3.54.5"},"reference-count":33,"publisher":"SAGE Publications","issue":"8","license":[{"start":{"date-parts":[[2021,1,18]],"date-time":"2021-01-18T00:00:00Z","timestamp":1610928000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Cereb Blood Flow Metab"],"published-print":{"date-parts":[[2021,8]]},"abstract":"<jats:p>\n                    Patients with Parkinson\u2019s disease (PD) often suffer from non-motor symptoms, which may be caused by serotonergic dysfunction. Apart from alleviating the motor symptoms, Deep Brain Stimulation (DBS) in the subthalamic nucleus (STN) may also influence non-motor symptoms. The aim of this study is to investigate how turning DBS off affects the serotonergic system. We here exploit a novel functional PET neuroimaging methodology to evaluate the preservation of serotonergic neurons and capacity to release serotonin. We measured cerebral 5-HT\n                    <jats:sub>1B<\/jats:sub>\n                    R binding in 13 DBS-STN treated PD patients, at baseline and after turning DBS off. Ten age-matched volunteers served as controls. Clinical measures of motor symptoms were assessed under the two conditions and correlated to the PET measures of the static and dynamic integrity of the serotonergic system. PD patients exhibited a significant loss of frontal and parietal 5-HT\n                    <jats:sub>1B<\/jats:sub>\n                    R, and the loss was significantly correlated to motor symptom severity. We saw a corresponding release of serotonin, but only in brain regions with preserved 5-HT\n                    <jats:sub>1B<\/jats:sub>\n                    R, suggesting the presence of a presynaptic serotonergic deficit. Our study demonstrates that DBS-STN dynamically regulates the serotonin system in PD, and that preservation of serotonergic functions may be predictive of DBS-STN effects.\n                  <\/jats:p>","DOI":"10.1177\/0271678x20982389","type":"journal-article","created":{"date-parts":[[2021,1,19]],"date-time":"2021-01-19T01:20:10Z","timestamp":1611019210000},"page":"1954-1963","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":28,"title":["Parkinson patients have a presynaptic serotonergic deficit: A dynamic deep brain stimulation PET study"],"prefix":"10.1177","volume":"41","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1009-7139","authenticated-orcid":false,"given":"Louise M","family":"J\u00f8rgensen","sequence":"first","affiliation":[{"name":"Neurobiology Research Unit, Department of Neurology, Rigshospitalet, Copenhagen, Denmark"},{"name":"Institute of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tove","family":"Henriksen","sequence":"additional","affiliation":[{"name":"Department of Neurology, Bispebjerg Hospital, Copenhagen, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Skirmante","family":"Mardosiene","sequence":"additional","affiliation":[{"name":"Department of Neurology, Bispebjerg Hospital, Copenhagen, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sune H","family":"Keller","sequence":"additional","affiliation":[{"name":"Department of Clinical Physiology, Nuclear Medicine and PET, Rigshospitalet, Copenhagen, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dea S","family":"Stenb\u00e6k","sequence":"additional","affiliation":[{"name":"Neurobiology Research Unit, Department of Neurology, Rigshospitalet, Copenhagen, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5564-7627","authenticated-orcid":false,"given":"Hanne D","family":"Hansen","sequence":"additional","affiliation":[{"name":"Neurobiology Research Unit, Department of Neurology, Rigshospitalet, Copenhagen, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bo","family":"Jespersen","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carsten","family":"Thomsen","sequence":"additional","affiliation":[{"name":"Department of Radiology, Rigshospitalet, University of Copenhagen, Denmark"},{"name":"Research Center for Advanced Imaging, Zealand University Hospital, Roskilde, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pia","family":"Weikop","sequence":"additional","affiliation":[{"name":"Center for Basic and Translational Neuroscience, Nedergaard Laboratory, Division of Glial Disease and Therapeutics, University of Copenhagen, Copenhagen, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7811-1825","authenticated-orcid":false,"given":"Claus","family":"Svarer","sequence":"additional","affiliation":[{"name":"Neurobiology Research Unit, Department of Neurology, Rigshospitalet, Copenhagen, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gitte M","family":"Knudsen","sequence":"additional","affiliation":[{"name":"Neurobiology Research Unit, Department of Neurology, Rigshospitalet, Copenhagen, Denmark"},{"name":"Institute of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, 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