Journal
JOURNAL OF PARKINSONS DISEASE
Volume 11, Issue 4, Pages 1569-1578Publisher
IOS PRESS
DOI: 10.3233/JPD-212657
Keywords
GBA; Parkinson's disease; motor complications; dyskinesias; motor fluctuations
Categories
Funding
- Research Council of Norway [177966, 287842]
- Western Norway Regional Health Authority [911218]
- Norwegian Parkinson's Research Foundation
- Rebergs Legacy
- Parkinson's UK [G0502, G0914, G1302]
- Scottish Government Chief Scientist Office
- BMA Doris Hillier Award
- BUPA Foundation
- NHS Grampian Endowments
- RS MacDonald Trust
- Swedish Medical Research Council
- Swedish Parkinson's disease Association
- Swedish Parkinson's Foundation
- Parkinson Research Foundation
- Erling Persson Foundation
- Kempe Foundation
- Swedish Brain Foundation (Hjarnfonden)
- Vasterbotten County Council
- NIH [F32AG063442]
- NIH/NIEHS [R01-ES010544, U54-ES012078]
- Michael J. Fox Foundation: 2021 RFA: Accelerating Publication of Parkinson's Disease Replication Data
Ask authors/readers for more resources
This study found no association between GBA carrier status and the risk of developing motor complications in Parkinson's disease patients. It is important to publish studies with null results to accurately summarize the clinical features of GBA-associated PD.
Background: Motor complications are a consequence of the chronic dopaminergic treatment of Parkinson's 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 = 0.30) or MF (HR 1.19, 95% CI 0.84 to 1.70, p = 0.33). 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 = 0.82) or MF (HR 1.22, 95% CI 0.74 to 2.04, p = 0.43). 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.
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