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. 2024 Aug 1;147(8):2652–2667. doi: 10.1093/brain/awae188

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© The Author(s) 2024. Published by Oxford University Press on behalf of the Guarantors of Brain.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Workflow for genetic analysis of the ROPAD study participants, indicating the numbers of analysed patients and the most relevant results. Numbers of individuals with variants in: (i) Parkinson’s disease (PD)-related genes (n = 2743); (ii) atypical parkinsonism genes (n = 973); (iii) dystonia–parkinsonism genes (n = 564); (iv) genes related to neurodegenerative disorders with prominent/predominant (atypical) parkinsonism (n = 470); (v) dystonia/dyskinesia-related genes (n = 1505); and (vi) dementia-related genes (n = 695) do not add up to the number of individuals with pathogenic (P)/likely pathogenic (LP)/PD-relevant risk factors (RFs)/variants of uncertain significance (VUS) detected by gene panel sequencing (n = 5361), given that these groups of patients partly overlap (e.g. some of the patients with variants in dystonia/dyskinesia-related genes also harbour variants in PD-related genes, etc.).