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

Journal of the International Neuropsychological Society - Tập 23 Số 2 - Trang 150-158 - 2017
Adolfo M. García1,2,3, Lucas Sedeño2,3, Natalia Trujillo4,5,6, Yamile Bocanegra4,6, Diana Gómez5,6, David Pineda4,6, Andrés Villegas6, Édinson Muñoz7, William Arias8, Agustín Ibáñez9,10,2,3,11
1Faculty of Elementary and Special Education (FEEyE), National University of Cuyo (UNCuyo), Mendoza, Argentina
2Laboratory of Experimental Psychology and Neuroscience (LPEN), Institute of Cognitive and Translational Neuroscience (INCyT), INECO Foundation, Favaloro University, Buenos Aires, Argentina
3National Scientific and Technical Research Council (CONICET), Buenos Aires, Argentina
4Group of Neuropsychology and Conduct (GRUNECO), Faculty of Medicine, University of Antioquia (UDEA), Medellín, Colombia
5Mental Health Group, School of Public Health, University of Antioquia (UDEA), Medellín, Colombia
6Neuroscience Group, Faculty of Medicine, University of Antioquia (UdeA), Medellín, Colombia
7Departamento de Lingüística y Literatura, Facultad de Humanidades, Universidad de Santiago de Chile, Santiago, Chile
8Molecular Genetics Laboratory, University of Antioquia (UDEA), Medellín, Colombia
9Center for Social and Cognitive Neuroscience (CSCN), School of Psychology, Universidad Adolfo Ibáñez, Santiago de Chile, Chile
10Centre of Excellence in Cognition and its Disorders, Australian Research Council (ACR), Macquarie University, Sydney, Australia
11Universidad Autónoma del Caribe, Barranquilla, Colombia

Tóm tắt

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 individualsat riskfor 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 detectsui generislanguage 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 thissui generisdisturbance 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)

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