Objective. Health comorbidities, particularly cardiovascular risk factors, are well known to pose risks for cognitive decline in older adults. To date, little attention has focused on the impact of these comorbidities on Parkinson’s disease (PD). This study examined the prevalence and contribution of comorbidities on cognitive status in PD patients, above and beyond the effects of disease severity. Methods. A cross sectional design was used, including neuropsychological data on 341 PD patients without severe cognitive decline. Comorbidity data were collected via medical chart review. Data were analyzed using a series of multiple hierarchical regressions, controlling for PD-related disease variables. Results. Overall sample characteristics are 69% male, disease duration 9.7 years, Unified Parkinson’s Disease Rating Scale 26.4, and age 64.7 years. Hypercholesterolemia (41.6%), hypertension (38.1%), and hypotension (30.2%) were the most reported comorbidities. The presence of hypertension significantly contributed to domains of executive function and verbal memory. The cooccurrence of orthostatic hypotension moderated the relationship between hypertension and executive function. Conclusions. This study on a large cohort of PD patients provides evidence for a detrimental influence of health comorbidities, particularly hypertension, on cognitive domains that have traditionally been conceptualized as being frontally and/or temporally mediated. 1. Introduction The overall goal of this proof of concept study was to learn whether cardiovascular risk factors, like hypertension and diabetes, might negatively influence cognitive status in Parkinson’s disease, similar to that observed in normal elderly. Parkinson’s disease (PD) is a complex multisystem disorder characterized by motor, cognitive, and mood-motivational changes [1, 2]. Particularly, insidious are cognitive changes. When initially diagnosed, 5–20% of PD patients show signs of cognitive difficulties and up to 80% become demented after 15–20 years [3, 4]. Typical cognitive changes include slowed processing (bradyphrenia), increased forgetfulness, and difficulty with multitasking and working memory. Cognitive changes can occur early in the disease course, worsen with disease progression, and detrimentally affect quality of life and survival [3, 5]. From a neural systems perspective, PD-related cognitive decline has been attributed to deregulation of dopamine-mediated frontal-striatal circuitry and is further complicated by cholinergic changes [6, 7]. Over the past decade, mounting evidence has pointed to
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