Language deficits as a preclinical window into Parkinson?s disease: Evidence from asymptomatic parkin and dardarin mutation carriers

GARCÍA, A. M., SEDEÑO, L., TRUJILLO, N., BOCANEGRA, Y., GOMEZ, D., PINEDA, D., VILLEGAS, A., ARIAS, W. & IBÁÑEZ, A

La Havana

Congreso; 18th World Congress of the International Organization of Psychophysiology; 2016

International Organization of Psychophysiology

The worldwide spread of Parkinson?s disease (PD) calls for sensitive and specific measures enabling its early (or, ideally, preclinical) detection. Here we employ language measures revealing deficits in PD to explore whether similar disturbances are present in asymptomatic individuals at risk for the disease. We administered executive, semantic, verb-production, and syntactic tasks to 33 sporadic PD patients, 8 genetic PD patients with parkin (PARK2) or dardarin (LRRK2) mutation, 9 asymptomatic first-degree relatives of the latter with similar mutations, and socio-demographically matched controls for the clinical and subclinical samples (N = 36 and 20, respectively). Demographic and experimental data were analyzed using ANOVA and Tukey?s HSD post-hoc tests (except for gender, which was analyzed via Pearson chi-square tests). Effect sizes were calculated with Eta squared (n2). Moreover, to detect sui generis language disturbances, we ran ANCOVA tests using executive functions as covariate. In all cases, alpha values were set at p < .05. The two clinical groups showed impairments in all measures (all p-values < .01, all effect sizes > 0.2) most of which survived covariation with executive functions. However, the key finding concerned asymptomatic mutation carriers. While these subjects showed intact executive (p = .25), semantic (p > .09), and action-verb production (p = .14) skills, they evinced deficits in a syntactic test with minimal working memory load (p < .01, n2 = .26). 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. [This work was partially supported by grants from CONICET, CONICYT/FONDECYT Regular (1130920), COLCIENCIAS (1115-545-31374 and 1115-569-33858), FONCyT-PICT 2012-0412, FONCyT-PICT 2012-1309, FONDAP 15150012, and INECO Foundation].