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Hypothalamic volume loss is associated with reduced melatonin output in Parkinson's disease

Lookup NU author(s): Professor David Burn, Professor David BrooksORCiD

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Abstract

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

Publication metadata

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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