Affiliations: [a] Somerville College, University of Oxford, Oxford, UK
| [b] The Edmond J. Safra Program in Parkinson’s Disease and the Morton and Gloria Shulman Movement Disorders Centre and, Toronto Western Hospital, Toronto, ON, Canada
| [c] Department of Medicine, Parkinson’s Disease and Movement Disorders Center, Division of Neurology, The Ottawa Hospital Research Institute, University of Ottawa Brain and Mind Institute, Ottawa, Canada
| [d] Usher Institute of Population Health Sciences and Informatics, University of Edinburgh, Edinburgh, UK
| [e] Department of Medicine, Division of Neurology, Hamilton Health Sciences, McMaster University, Hamilton, ON, Canada
| [f] Department of Neurology, Movement Disorders Center, University of Colorado, Anschutz Medical Campus, Aurora, CO, USA
| [g] Engineering and Applied Science, Aston University, Birmingham, UK
| [h] Media Lab, Massachusetts Institute of Technology, Cambridge, MA, USA
Correspondence to: Connie Marras, MD, PhD, 84 Queen’s Park, Toronto, ON M5S 2C5, Canada. Tel.: +1 416 603 6422; E-mail: [email protected].
Note:  These authors contributed equally to this work.
Abstract: We investigate the potential association between leucine-rich repeat kinase 2 (LRRK2) mutations and voice. Sustained phonations (‘aaah’ sounds) were recorded from 7 individuals with LRRK2-associated Parkinson’s disease (PD), 17 participants with idiopathic PD (iPD), 20 non-manifesting LRRK2-mutation carriers, 25 related non-carriers, and 26 controls. In distinguishing LRRK2-associated PD and iPD, the mean sensitivity was 95.4% (SD 17.8%) and mean specificity was 89.6% (SD 26.5%). Voice features for non-manifesting carriers, related non-carriers, and controls were much less discriminatory. Vocal deficits in LRRK2-associated PD may be different than those in iPD. These preliminary results warrant longitudinal analyses and replication in larger cohorts.