. 2025 Jan:130:107191.

doi: 10.1016/j.parkreldis.2024.107191. Epub 2024 Oct 31.

GBA1 T369M and Parkinson's disease - Further evidence of a lack of association in the Swedish population

Kajsa Atterling Brolin¹, David Bäckström², Joel Wallenius³, Ziv Gan-Or⁴, Andreas Puschmann⁵, Oskar Hansson⁶, Maria Swanberg⁷

Affiliations

¹ Translational Neurogenetics Unit, Department of Experimental Medical Science, Lund University, Lund, Sweden; Centre for Preventive Neurology, Wolfson Institute of Population Health, Queen Mary University of London, EC1M 6BQ, London, UK. Electronic address: kajsa.brolin@med.lu.se.
² Department of Clinical Science, Neurosciences, Umeå University, Umeå, Sweden.
³ Division of Neurology, Department of Clinical Sciences Lund, Lund University, Lund, Sweden; Department of Neurology, Skåne University Hospital, Lund, Sweden.
⁴ Department of Neurology & Neurosurgery, McGill University, Montreal, Quebec, Canada; Clinical Research Unit, The Neuro (Montreal Neurological Institute-Hospital), Montreal, Quebec, Canada; Department of Human Genetics, McGill University, Montreal, Quebec, Canada.
⁵ Division of Neurology, Department of Clinical Sciences Lund, Lund University, Lund, Sweden; Department of Neurology, Skåne University Hospital, Lund, Sweden; SciLifeLab National Research Infrastructure, Lund University, Sweden.
⁶ Clinical Memory Research Unit, Department of Clinical Sciences Malmö, Faculty of Medicine, Lund University, Lund, Sweden; Memory Clinic, Skåne University Hospital, Malmö, Sweden.
⁷ Translational Neurogenetics Unit, Department of Experimental Medical Science, Lund University, Lund, Sweden.

PMID: 39514913
DOI: 10.1016/j.parkreldis.2024.107191

Free article

GBA1 T369M and Parkinson's disease - Further evidence of a lack of association in the Swedish population

Kajsa Atterling Brolin et al. Parkinsonism Relat Disord. 2025 Jan.

Free article

. 2025 Jan:130:107191.

doi: 10.1016/j.parkreldis.2024.107191. Epub 2024 Oct 31.

Authors

Kajsa Atterling Brolin¹, David Bäckström², Joel Wallenius³, Ziv Gan-Or⁴, Andreas Puschmann⁵, Oskar Hansson⁶, Maria Swanberg⁷

Affiliations

¹ Translational Neurogenetics Unit, Department of Experimental Medical Science, Lund University, Lund, Sweden; Centre for Preventive Neurology, Wolfson Institute of Population Health, Queen Mary University of London, EC1M 6BQ, London, UK. Electronic address: kajsa.brolin@med.lu.se.
² Department of Clinical Science, Neurosciences, Umeå University, Umeå, Sweden.
³ Division of Neurology, Department of Clinical Sciences Lund, Lund University, Lund, Sweden; Department of Neurology, Skåne University Hospital, Lund, Sweden.
⁴ Department of Neurology & Neurosurgery, McGill University, Montreal, Quebec, Canada; Clinical Research Unit, The Neuro (Montreal Neurological Institute-Hospital), Montreal, Quebec, Canada; Department of Human Genetics, McGill University, Montreal, Quebec, Canada.
⁵ Division of Neurology, Department of Clinical Sciences Lund, Lund University, Lund, Sweden; Department of Neurology, Skåne University Hospital, Lund, Sweden; SciLifeLab National Research Infrastructure, Lund University, Sweden.
⁶ Clinical Memory Research Unit, Department of Clinical Sciences Malmö, Faculty of Medicine, Lund University, Lund, Sweden; Memory Clinic, Skåne University Hospital, Malmö, Sweden.
⁷ Translational Neurogenetics Unit, Department of Experimental Medical Science, Lund University, Lund, Sweden.

PMID: 39514913
DOI: 10.1016/j.parkreldis.2024.107191

Abstract

Variants in GBA1 are important genetic risk factors in Parkinson's disease (PD). GBA1 T369M has been linked to an ∼80 % increased PD risk but the reports are conflicting and the relevance of GBA1 variants in different populations varies. A lack of association between T369M and PD in the Swedish population was recently reported but needs further validation. We therefore investigated T369M in 1,808 PD patients and 2,183 controls and our results support that T369M is not a risk factor for PD in the Swedish population.

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Conflict of interest statement

Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests:Z.G received consultancy fees from Lysosomal Therapeutics Inc. (LTI), Idorsia, Prevail Therapeutics, Ono Therapeutics, Denali, Handl Therapeutics, Neuron23, Bial Biotech, Bial, UCB, Capsida, Vanqua bio, Congruence Therapeutics, Takeda, Jazz pharmaceuticals, Guidepoint, Lighthouse and Deerfield. O.H. has acquired research support (for the institution) from AVID Radiopharmaceuticals, Biogen, C2N Diagnostics, Eli Lilly, Eisai, Fujirebio, GE Healthcare, and Roche. In the past 2 years, he has received consultancy/speaker fees from AC Immune, Alzpath, BioArctic, Biogen, Bristol Meyer Squibb, Cerveau, Eisai, Eli Lilly, Fujirebio, Merck, Novartis, Novo Nordisk, Roche, Sanofi and Siemens.

Update of

Is GBA1 T369M not a risk factor for Parkinson's disease in the Swedish population?
Brolin KA, Bäckström D, Wallenius J, Gan-Or Z, Puschmann A, Hansson O, Swanberg M. Brolin KA, et al. medRxiv [Preprint]. 2024 Mar 16:2024.03.15.24304347. doi: 10.1101/2024.03.15.24304347. medRxiv. 2024. Update in: Parkinsonism Relat Disord. 2025 Jan;130:107191. doi: 10.1016/j.parkreldis.2024.107191. PMID: 38559109 Free PMC article. Updated. Preprint.

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GBA1 T369M and Parkinson's disease - Further evidence of a lack of association in the Swedish population

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GBA1 T369M and Parkinson's disease - Further evidence of a lack of association in the Swedish population

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