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语言缺陷作为帕金森病临床前的一个窗口:来自无症状帕金蛋白和多巴胺能突变携带者的证据。

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

作者信息

García Adolfo M, Sedeño Lucas, Trujillo Natalia, Bocanegra Yamile, Gomez Diana, Pineda David, Villegas Andrés, Muñoz Edinson, Arias William, Ibáñez Agustín

机构信息

1Laboratory of Experimental Psychology and Neuroscience (LPEN),Institute of Cognitive and Translational Neuroscience (INCyT),INECO Foundation,Favaloro University,Buenos Aires,Argentina.

4Mental Health Group,School of Public Health,University of Antioquia (UDEA),Medellín,Colombia.

出版信息

J Int Neuropsychol Soc. 2017 Feb;23(2):150-158. doi: 10.1017/S1355617716000710.

DOI:10.1017/S1355617716000710
PMID:28205494
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).

摘要

目的

帕金森病(PD)在全球范围内的传播需要灵敏且特异的措施以实现其早期(或理想情况下的临床前)检测。在此,我们使用揭示PD语言缺陷的测量方法,来探究在有患该疾病风险的无症状个体中是否存在类似的语言障碍。

方法

我们对散发型PD患者、携带PARK2(帕金森蛋白)或LRRK2(富含亮氨酸重复激酶2)突变的遗传性PD患者、具有相似突变的后者的无症状一级亲属以及社会人口统计学匹配的对照组进行了执行功能、语义、动词生成和句法任务测试。此外,为了检测独特的语言障碍,我们使用执行功能作为协变量进行了协方差分析测试。

结果

两个临床组在所有测量中均表现出损伤,其中大多数在与执行功能的协变量分析后仍存在。然而,关键发现涉及无症状突变携带者。虽然这些受试者的执行功能、语义和动作动词生成技能完好,但他们在一个工作记忆负荷极小的句法测试中表现出缺陷。

结论

我们提出这种独特的障碍可能构成PD最终发展的前驱迹象。此外,我们的结果表明,影响基底神经节功能的特定基因(PARK2和LRRK2)上的突变可能与语言处理机制存在微妙关联。(《神经心理学报》,2017年,第23卷,第150 - 158页)

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