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Lookup NU author(s): Professor David BurnORCiD, Professor David BrooksORCiD
This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).
BackgroundRecent studies have suggested that melatonina hormone produced by the pineal gland under circadian controlcontributes to PD-related sleep dysfunction. We hypothesized that degenerative changes to the neural structures controlling pineal function (especially the suprachiasmatic nuclei of the anterior hypothalamus) may be responsible for reduced melatonin output in these patients. We compared hypothalamic volumes in PD patients with matched controls and determined whether volume loss correlated with reduced melatonin output in the PD group.MethodsA total of 12 PD patients and 12 matched controls underwent magnetic resonance imaging to determine hypothalamic volume. In addition, PD patients underwent 24-hour blood sampling in a controlled environment to determine serum melatonin concentrations using enzyme-linked immunosorbent assays.ResultsPD patients had significantly reduced hypothalamic gray matter volume when compared with matched controls. Melatonin levels were significantly associated with hypothalamic gray matter volume and disease severity in PD patients.ConclusionMelatonin levels are associated with hypothalamic gray matter volume loss and disease severity in PD patients. This provides anatomical and physiological support for an intrinsic sleep and circadian phenotype in PD. (c) 2016 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society
Author(s): Breen DP, Nombela C, Vuono R, Jones PS, Fisher K, Burn DJ, Brooks DJ, Reddy AB, Rowe JB, Barker RA
Publication type: Article
Publication status: Published
Journal: Movement Disorders
Year: 2016
Volume: 31
Issue: 7
Pages: 1062-1066
Print publication date: 01/07/2016
Online publication date: 12/03/2016
Acceptance date: 03/02/2016
Date deposited: 02/09/2016
ISSN (print): 0885-3185
ISSN (electronic): 1531-8257
Publisher: Wiley-Blackwell
URL: http://dx.doi.org/10.1002/mds.26592
DOI: 10.1002/mds.26592
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