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Language Deficits as a Preclinical Window into Parkinson’s Disease: Evidence from Asymptomatic Parkin and Dardarin Mutation Carriers

Published online by Cambridge University Press:  16 February 2017

Adolfo M. García
Affiliation:
Laboratory of Experimental Psychology and Neuroscience (LPEN), Institute of Cognitive and Translational Neuroscience (INCyT), INECO Foundation, Favaloro University, Buenos Aires, Argentina National Scientific and Technical Research Council (CONICET), Buenos Aires, Argentina Faculty of Elementary and Special Education (FEEyE), National University of Cuyo (UNCuyo), Mendoza, Argentina
Lucas Sedeño
Affiliation:
Laboratory of Experimental Psychology and Neuroscience (LPEN), Institute of Cognitive and Translational Neuroscience (INCyT), INECO Foundation, Favaloro University, Buenos Aires, Argentina National Scientific and Technical Research Council (CONICET), Buenos Aires, Argentina
Natalia Trujillo
Affiliation:
Mental Health Group, School of Public Health, University of Antioquia (UDEA), Medellín, Colombia Group of Neuropsychology and Conduct (GRUNECO), Faculty of Medicine, University of Antioquia (UDEA), Medellín, Colombia Neuroscience Group, Faculty of Medicine, University of Antioquia (UDEA), Medellín, Colombia
Yamile Bocanegra
Affiliation:
Group of Neuropsychology and Conduct (GRUNECO), Faculty of Medicine, University of Antioquia (UDEA), Medellín, Colombia Neuroscience Group, Faculty of Medicine, University of Antioquia (UDEA), Medellín, Colombia
Diana Gomez
Affiliation:
Mental Health Group, School of Public Health, University of Antioquia (UDEA), Medellín, Colombia Neuroscience Group, Faculty of Medicine, University of Antioquia (UDEA), Medellín, Colombia
David Pineda
Affiliation:
Group of Neuropsychology and Conduct (GRUNECO), Faculty of Medicine, University of Antioquia (UDEA), Medellín, Colombia Neuroscience Group, Faculty of Medicine, University of Antioquia (UDEA), Medellín, Colombia
Andrés Villegas
Affiliation:
Neuroscience Group, Faculty of Medicine, University of Antioquia (UDEA), Medellín, Colombia
Edinson Muñoz
Affiliation:
Departamento de Lingüística y Literatura, Facultad de Humanidades, Universidad de Santiago de Chile, Santiago, Chile
William Arias
Affiliation:
Molecular Genetics Laboratory, University of Antioquia (UDEA), Medellín, Colombia
Agustín Ibáñez*
Affiliation:
Laboratory of Experimental Psychology and Neuroscience (LPEN), Institute of Cognitive and Translational Neuroscience (INCyT), INECO Foundation, Favaloro University, Buenos Aires, Argentina National Scientific and Technical Research Council (CONICET), Buenos Aires, Argentina Universidad Autónoma del Caribe, Barranquilla, Colombia Center for Social and Cognitive Neuroscience (CSCN), School of Psychology, Universidad Adolfo Ibáñez, Santiago de Chile, Chile Centre of Excellence in Cognition and its Disorders, Australian Research Council (ACR), Macquarie University, Sydney, Australia
*
Correspondence and reprint requests to: Agustín Ibáñez, Institute of Cognitive and Translational Neuroscience & CONICET; Pacheco de Melo 1860, C1126AAB, Buenos Aires, Argentina. E-mail: aibanez@ineco.org.ar

Abstract

Objectives: The worldwide spread of Parkinson’s disease (PD) calls for sensitive and specific measures enabling its early (or, ideally, preclinical) detection. Here, we use language measures revealing deficits in PD to explore whether similar disturbances are present in asymptomatic individuals at risk for the disease. Methods: We administered executive, semantic, verb-production, and syntactic tasks to sporadic PD patients, genetic PD patients with PARK2 (parkin) or LRRK2 (dardarin) mutation, asymptomatic first-degree relatives of the latter with similar mutations, and socio-demographically matched controls. Moreover, to detect sui generis language disturbances, we ran analysis of covariance tests using executive functions as covariate. Results: The two clinical groups showed impairments in all measures, most of which survived covariation with executive functions. However, the key finding concerned asymptomatic mutation carriers. While these subjects showed intact executive, semantic, and action-verb production skills, they evinced deficits in a syntactic test with minimal working memory load. Conclusions: We propose that this sui generis disturbance may constitute a prodromal sign anticipating eventual development of PD. Moreover, our results suggest that mutations on specific genes (PARK2 and LRRK2) compromising basal ganglia functioning may be subtly related to language-processing mechanisms. (JINS, 2017, 23, 150–158)

Type
Research Articles
Copyright
Copyright © The International Neuropsychological Society 2017 

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