학술논문

The relationship between obsessive‐compulsive symptoms and PARKIN genotype: The CORE‐PD study
Document Type
article
Source
Movement Disorders. 30(2)
Subject
Biomedical and Clinical Sciences
Oncology and Carcinogenesis
Brain Disorders
Parkinson's Disease
Neurodegenerative
Genetics
Neurosciences
2.1 Biological and endogenous factors
Aetiology
Neurological
Adult
Age of Onset
Aged
Female
Genetic Predisposition to Disease
Genetic Testing
Genotype
Heterozygote
Humans
Male
Middle Aged
Mutation
Obsessive-Compulsive Disorder
Parkinson Disease
Ubiquitin-Protein Ligases
Parkinson's
neuropsychological
obsessive-compulsive
parkin
Clinical Sciences
Human Movement and Sports Sciences
Neurology & Neurosurgery
Clinical sciences
Language
Abstract
BackgroundFew studies have systematically investigated the association between PARKIN genotype and psychiatric co-morbidities of Parkison's disease (PD). PARKIN-associated PD is characterized by severe nigral dopaminergic neuronal loss, a finding that may have implications for behaviors rooted in dopaminergic circuits such as obsessive-compulsive symptoms (OCS).MethodsThe Schedule of Compulsions and Obsessions Patient Inventory (SCOPI) was administered to 104 patients with early-onset PD and 257 asymptomatic first-degree relatives. Carriers of one and two PARKIN mutations were compared with noncarriers.ResultsAmong patients, carriers scored lower than noncarriers in adjusted models (one-mutation: 13.9 point difference, P = 0.03; two-mutation: 24.1, P = 0.001), where lower scores indicate less OCS. Among asymptomatic relatives, a trend toward the opposite was seen: mutation carriers scored higher than noncarriers (one mutation, P = 0.05; two mutations, P = 0.13).ConclusionsFirst, a significant association was found between PARKIN mutation status and obsessive-compulsive symptom level in both PD and asymptomatic patients, suggesting that OCS might represent an early non-motor dopamine-dependent feature. Second, irrespective of disease status, heterozygotes were significantly different from noncarriers, suggesting that PARKIN heterozygosity may contribute to phenotype. © 2014 International Parkinson and Movement Disorder Society.