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Vol. 11, No. 2, 2013
Issue release date: November 2012
Section title: Paper
Neurodegenerative Dis 2013;11:72–78
(DOI:10.1159/000341997)

Delay Discounting of Reward and Caudate Nucleus Volume in Individuals with α-Synuclein Gene Duplication before and after the Development of Parkinson’s Disease

Szamosi A. · Nagy H. · Kéri S.
aNational Psychiatry Center, bNational Institute for Medical Rehabilitation, and cDepartment of Neurology, Semmelweis University, Budapest, and dDepartment of Physiology, Faculty of Medicine, University of Szeged, Szeged, Hungary

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Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: 10/3/2012

Number of Print Pages: 7
Number of Figures: 5
Number of Tables: 1

ISSN: 1660-2854 (Print)
eISSN: 1660-2862 (Online)

For additional information: http://www.karger.com/NDD

Abstract

Background/Aims: α-Synuclein (SNCA) may be a key factor in dopaminergic neurotransmission, reward processing, and neurodegeneration in Parkinson’s disease (PD). We investigated delay discounting of reward and caudate volume in SNCA gene duplication carriers before and after the development of PD. Methods: Participants were 7 presymptomatic SNCA duplication carriers who later developed PD (follow-up period: 5.4 years) and 10 matched non-carrier controls. At the follow-up assessment, patients received levodopa (l-DOPA) therapy. Delay discounting of reward was assessed with the Kirby discounting questionnaire. We measured the volume of the caudate nucleus and cerebral cortex using structural MRI and FreeSurfer software. Results: In the presymptomatic stage, carriers showed similar delay discounting and caudate volume to that of non-carrier controls. However, after the development of PD, we observed a significant elevation in delay discounting (impulsive decisions) and reduced caudate volume. There was no cortical atrophy. Conclusion: Impaired reward-related decision making and caudate volume loss are not detectable in the presymptomatic stage in SNCA duplication carriers. These behavioral and neuroanatomical alterations are observed after the development of clinical symptoms when there is extensive neurodegeneration. Study limitations include a small sample size as well as the potential confounding effect of general cognitive decline.


  

Author Contacts

Dr. Szabolcs Kéri
Department of Physiology, Faculty of Medicine
University of Szeged
HU–6720 Szeged (Hungary)
E-Mail szkeri2000@yahoo.com or keri.szabolcs.gyula@med.u-szeged.hu

  

Article Information

Published online: October 3, 2012
Number of Print Pages : 7
Number of Figures : 5, Number of Tables : 1, Number of References : 39

  

Publication Details

Neurodegenerative Diseases

Vol. 11, No. 2, Year 2013 (Cover Date: November 2012)

Journal Editor: Nitsch R.M. (Zürich), Hock C. (Zürich)
ISSN: 1660-2854 (Print), eISSN: 1660-2862 (Online)

For additional information: http://www.karger.com/NDD


Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: 10/3/2012

Number of Print Pages: 7
Number of Figures: 5
Number of Tables: 1

ISSN: 1660-2854 (Print)
eISSN: 1660-2862 (Online)

For additional information: http://www.karger.com/NDD


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