{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T09:56:40Z","timestamp":1777888600709,"version":"3.51.4"},"reference-count":48,"publisher":"SAGE Publications","issue":"4","license":[{"start":{"date-parts":[[2021,10,12]],"date-time":"2021-10-12T00:00:00Z","timestamp":1633996800000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JPD"],"published-print":{"date-parts":[[2021,10,12]]},"abstract":"<jats:p>Background: Motor complications are a consequence of the chronic dopaminergic treatment of Parkinson\u2019s disease (PD) and include levodopa-induced dyskinesia (LIDs) and motor fluctuations (MF). Currently, evidence is on lacking whether patients with GBA-associated PD differ in their risk of developing motor complications compared to the general PD population. Objective: To evaluate the association of GBA carrier status with the development of LIDS and MFs from early PD. Methods: Motor complications were recorded prospectively in 884 patients with PD from four longitudinal cohorts using part IV of the UPDRS or MDS-UPDRS. Subjects were followed for up to 11 years and the associations of GBA mutations with the development of motor complications were assessed using parametric accelerated failure time models. Results: In 439 patients from Europe, GBA mutations were detected in 53 (12.1%) patients and a total of 168 cases of LIDs and 258 cases of MF were observed. GBA carrier status was not associated with the time to develop LIDs (HR 0.78, 95%CI 0.47 to 1.26, p\u200a=\u200a0.30) or MF (HR 1.19, 95%CI 0.84 to 1.70, p\u200a=\u200a0.33). In the American cohorts, GBA mutations were detected in 36 (8.1%) patients and GBA carrier status was also not associated with the progression to LIDs (HR 1.08, 95%CI 0.55 to 2.14, p\u200a=\u200a0.82) or MF (HR 1.22, 95%CI 0.74 to 2.04, p\u200a=\u200a0.43). Conclusion: This study does not provide evidence that GBA-carrier status is associated with a higher risk of developing motor complications. Publication of studies with null results is vital to develop an accurate summary of the clinical features that impact patients with GBA-associated PD.<\/jats:p>","DOI":"10.3233\/jpd-212657","type":"journal-article","created":{"date-parts":[[2021,7,16]],"date-time":"2021-07-16T10:27:08Z","timestamp":1626431228000},"page":"1569-1578","source":"Crossref","is-referenced-by-count":8,"title":["Lack of Association Between GBA Mutations and Motor Complications in European and American Parkinson\u2019s Disease Cohorts"],"prefix":"10.1177","volume":"11","author":[{"given":"Jodi","family":"Maple-Gr\u00f8dem","sequence":"first","affiliation":[{"name":"The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway"},{"name":"Department of Chemistry, Bioscience and Environmental Engineering, University of Stavanger, Stavanger, Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kimberly C.","family":"Paul","sequence":"additional","affiliation":[{"name":"Department of Neurology, David Geffen School of Medicine, Los Angeles, CA, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ingvild","family":"Dalen","sequence":"additional","affiliation":[{"name":"Department of Research, Section of Biostatistics, Stavanger University Hospital, Stavanger, Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kathie J.","family":"Ngo","sequence":"additional","affiliation":[{"name":"Department of Neurology, David Geffen School of Medicine, Los Angeles, CA, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Darice","family":"Wong","sequence":"additional","affiliation":[{"name":"Department of Neurology, David Geffen School of Medicine, Los Angeles, CA, USA"},{"name":"Clinical Neurogenomics Research Center, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Angus D.","family":"Macleod","sequence":"additional","affiliation":[{"name":"Institute of Applied Health Sciences, University of Aberdeen, Aberdeen, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Carl E.","family":"Counsell","sequence":"additional","affiliation":[{"name":"Institute of Applied Health Sciences, University of Aberdeen, Aberdeen, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David","family":"B\u00e4ckstr\u00f6m","sequence":"additional","affiliation":[{"name":"Department of Clinical Science, Neurosciences, Ume\u00e5 University, Ume\u00e5, Sweden"},{"name":"Department of Neurology, and Department of Neuroscience, Yale University School of Medicine, New Haven, CT, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lars","family":"Forsgren","sequence":"additional","affiliation":[{"name":"Department of Clinical Science, Neurosciences, Ume\u00e5 University, Ume\u00e5, Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ole-Bj\u00f8rn","family":"Tysnes","sequence":"additional","affiliation":[{"name":"Department of Neurology, Haukeland University Hospital, Bergen, Norway"},{"name":"Department of Clinical Medicine, University of Bergen, Bergen, Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Cynthia D.J.","family":"Kusters","sequence":"additional","affiliation":[{"name":"Department of Human Genetics, University of California Los Angeles, Los Angeles, CA, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Brent L.","family":"Fogel","sequence":"additional","affiliation":[{"name":"Department of Neurology, David Geffen School of Medicine, Los Angeles, CA, USA"},{"name":"Clinical Neurogenomics Research Center, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jeff 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