{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,13]],"date-time":"2026-08-13T14:45:05Z","timestamp":1786632305455,"version":"build-2736575974"},"reference-count":28,"publisher":"Wiley","issue":"13","license":[{"start":{"date-parts":[[2013,7,11]],"date-time":"2013-07-11T00:00:00Z","timestamp":1373500800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2013,7,11]],"date-time":"2013-07-11T00:00:00Z","timestamp":1373500800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Movement Disorders"],"published-print":{"date-parts":[[2013,11]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Microglia are resident immunosurveillant cells in the central nervous system, and astrocytes are important for blood flow, plasticity, and neurotransmitter regulation. The aim of this study was to investigate whether astrocyte and microglial activation, estimated through markers in cerebrospinal fluid and serum, differed between synucleinopathies, tauopathies, and controls.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We analyzed the glial activation markers YKL\u201040 and soluble CD14 in serum and cerebrospinal fluid from 37 controls, 50 patients with Parkinson's disease (PD), and 79 P+ patients (those with progressive supranuclear palsy, corticobasal degeneration, and multiple system atrophy).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Cerebrospinal fluid levels of YKL\u201040 were decreased significantly in patients who had PD compared with controls (\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&lt;\u20090.05), patients who had multiple system atrophy (\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&lt;\u20090.01), and patients who had tauopathies (\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&lt;\u20090.0001). In addition, cerebrospinal fluid levels of YKL\u201040 were significantly lower in patients who had synucleinopathies than in those who had tauopathies (\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&lt;\u20090.0001).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>The decreased cerebrospinal fluid levels of YKL\u201040 suggest that glial activation is reduced in the brains of patients who have Parkinson's disease and synucleinopathies compared with patients who have tauopathies and controls. \u00a9 2013 International\nParkinson and Movement Disorder Society<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/mds.25589","type":"journal-article","created":{"date-parts":[[2013,7,11]],"date-time":"2013-07-11T10:48:38Z","timestamp":1373539718000},"page":"1882-1885","source":"Crossref","is-referenced-by-count":47,"title":["The glial marker YKL\u201040 is decreased in synucleinopathies"],"prefix":"10.1002","volume":"28","author":[{"given":"Bob","family":"Olsson","sequence":"first","affiliation":[{"name":"Department of Psychiatry and Neurochemistry the Sahlgrenska Academy at the University of Gothenburg M\u00f6lndal Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Radu","family":"Constantinescu","sequence":"additional","affiliation":[{"name":"Department of Neurology the Sahlgrenska Academy at the University of Gothenburg Gothenburg Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bj\u00f6rn","family":"Holmberg","sequence":"additional","affiliation":[{"name":"Department of Neurology the Sahlgrenska Academy at the University of Gothenburg Gothenburg Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Niels","family":"Andreasen","sequence":"additional","affiliation":[{"name":"Alzheimer Disease Research Center Karolinska Institute Stockhom Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kaj","family":"Blennow","sequence":"additional","affiliation":[{"name":"Department of Psychiatry and Neurochemistry the Sahlgrenska Academy at the University of Gothenburg M\u00f6lndal Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Henrik","family":"Zetterberg","sequence":"additional","affiliation":[{"name":"Department of Psychiatry and Neurochemistry the Sahlgrenska Academy at the University of Gothenburg M\u00f6lndal Sweden"},{"name":"University College London Institute of Neurology London United 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