The relationship between obsessive‐compulsive symptoms and PARKIN genotype: The CORE‐PD study. Issue 2 (12th November 2014)

• Record Type: Journal Article
• Authors: Sharp, Madeleine E.; Caccappolo, Elise; Mejia‐Santana, Helen; Tang, Ming‐X.; Rosado, Llency; Orbe Reilly, Martha; Ruiz, Diana; Louis, Elan D.; Comella, Cynthia; Nance, Martha; Bressman, Susan; Scott, William K.; Tanner, Caroline; Waters, Cheryl; Fahn, Stanley; Cote, Lucien; Ford, Blair; Rezak, Michael; Novak, Kevin; Friedman, Joseph H.; Pfeiffer, Ronald; Payami, Haydeh; Molho, Eric; Factor, Stuart A.; Nutt, John; Serrano, Carmen; Arroyo, Maritza; Pauciulo, Michael W.; Nichols, William C.; Clark, Lorraine N.; Alcalay, Roy N.; Marder, Karen S.; Stacy (Chair), Mark; Lang, Anthony; Napier, Celeste; Samuel, Michael; Strafella, Antonio; Weintraub, Daniel;
• Is Part Of: Movement disorders. Volume 30:Issue 2(2015)
• Page Start: 278
• Page End: 283
• Publication Date: 2014-11-12
• Subjects: Movement disorders -- Periodicals; 610
• DOI: 10.1002/mds.26065
• Languages: English
• ISSNs: 0885-3185

Abstract

<abstract abstract-type="main"> <title>ABSTRACT</title> <sec id="mds26065-sec-0001" sec-type="section"> <title>Background</title> <p>Few studies have systematically investigated the association between <italic>PARKIN</italic> genotype and psychiatric co‐morbidities of Parkison's disease (PD). <italic>PARKIN</italic>‐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).</p> </sec> <sec id="mds26065-sec-0002" sec-type="section"> <title>Methods</title> <p>The 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 <italic>PARKIN</italic> mutations were compared with noncarriers.</p> </sec> <sec id="mds26065-sec-0003" sec-type="section"> <title>Results</title> <p>Among patients, carriers scored lower than noncarriers in adjusted models (one‐mutation: 13.9 point difference, <italic>P</italic> = 0.03; two‐mutation: 24.1, <italic>P</italic> = 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, <italic>P</italic> = 0.05; two mutations, <italic>P</italic> = 0.13).</p> </sec> <sec id="mds26065-sec-0004" sec-type="section"> <title>Conclusions</title> <p>First, a significant association was found between <italic>PARKIN</italic> 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 <italic>PARKIN</italic> heterozygosity may contribute to phenotype. © 2014 International Parkinson and Movement Disorder Society</p> </sec> </abstract>