Genetic Influences on Cognition in Idiopathic Parkinson's Disease.

Abstract

Cognitive impairment in Parkinson's disease was clearly reported in the medical literature [1, 2]. This impairment is common to some degree even in nondemented Parkinson’s disease patients (PD-ND) and eventually progresses to dementia in 24 to 31% of patients [3]. The cognitive changes in PD are characterized by a frontalsubcortical impairment with decreased attention and executive function leading to progressive impairment in prefrontal tasks, visuospatial skills, and memory. Still, 20 to 25% of PDND patients may exhibit a pattern of cortical impairment with memory tasks and confrontation naming defects, and cognitive findings associated with cortical pathology, such as language errors, develop in many patients with PD with dementia (PDD) [4]. The identification of the biomarkers for cognitive impairment in patients with PD will allow better assessment of the patients' prognosis. Some genes, such as apolipoprotein E (ApoE) and microtubule-associated protein tau (MAPT), are of particular interest because of their known association with dementia in other neurodegenerative diseases, such as Alzheimer’s disease (AD) and atypical parkinsonian syndromes, including progressive supranuclear palsy and corticobasal degeneration (Morley et al., 2012) [5]. The aim of this study is to determine the role of genetic factors associated with cognitive decline in Parkinson’s disease (PD). We examined whether variations in apolipoprotein E (ApoE) and microtubule-associated protein tau (MAPT) genotypes are associated with cognitive decline in PD.