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Mov Disord. 2019 Dec 16. doi: 10.1002/mds.27945. [Epub ahead of print]

Metabolic correlates of dopaminergic loss in dementia with lewy bodies.

Author information

1
Department of Nuclear Medicine, University Hospital of Munich, LMU Munich, Munich, Germany.
2
Department of Neurology, University Hospital of Munich, LMU Munich, Munich, Germany.
3
Department of Psychiatry and Psychotherapy, University Hospital, LMU Munich, Munich, Germany.
4
Department of Radiology, University Hospital of Munich, LMU Munich, Munich, Germany.
5
IRCCS Ospedale Policlinico San Martino, Genoa, Italy.
6
Nuclear Medicine Unit, Department of Health Sciences, University of Genoa, Genoa, Italy.
7
National Institute of Nuclear Physics (INFN), Genoa section, Genoa, Genoa, Italy.
8
Department of Neurosciences, Faculty of Medicine, KU Leuven, Leuven, Belgium.
9
Department of Neurology, University Hospitals Leuven, Leuven, Belgium.
10
Department of Nuclear Medicine, University Hospitals Leuven, Leuven, Belgium.
11
Department of Neurology, University Medical Centre, Ljubljana, Slovenia.
12
Department for Nuclear Medicine, University Medical Centre, Ljubljana, Slovenia.
13
Division of Nuclear Medicine and Molecular Imaging, Geneva University Hospitals and NIMTLab, Geneva University, Geneva, Switzerland.
14
Department of Clinical Neurosciences, Geneva University Hospitals, Switzerland.
15
Department of Psychiatry, University of Cambridge, Cambridge, United Kingdom.
16
LANVIE (Laboratoire de Neuroimagerie du Vieillissement), Department of Psychiatry, Geneva University Hospitals, Geneva, Switzerland.
17
VU Medical Center Alzheimer Center, Amsterdam, The Netherlands.
18
Neurology Unit, University of Brescia, Brescia, Italy.
19
Parkinson's Disease Rehabilitation Centre, FERB ONLUS-S. Isidoro Hospital, Trescore Balneario (BG), Italy.
20
Division of Clinical Geriatrics, Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden.
21
Internal Medicine, section for Neurology, Sädersjukhuset, Stockholm, Sweden.
22
Medical Radiation Physics and Nuclear Medicine, Karolinska University Hospital, Stockholm, Sweden.
23
Department of Clinical Physiology, Institution of Medicine and Health Sciences, Linköping University Hospital, Linköping, Sweden.
24
Department of Diagnostic Radiology, Linköping University Hospital, Linköping, Sweden.
25
Center for Medical Image Science and Visualization (CMIV), Linköping University, Linköping, Sweden.
26
Servicio de Medicina Nuclear, Hospital de la Santa Creu i Sant Pau, Universitat Autònoma de Barcelona, Barcelona, España.
27
Clinical Neurology, Department of Neuroscience (DINOGMI), University of Genoa, Genoa, Italy.
28
DZNE-German Center for Neurodegenerative Diseases, Munich, Germany.
29
Ageing Epidemiology Research Unit (AGE), School of Public Health, Imperial College, London, United Kingdom.
30
Institut for Stroke and Dementia Research, University of Munich, Munich, Germany.
31
Munich Cluster for Systems Neurology (SyNergy), Munich, Germany.
32
Department of Nuclear Medicine, University of Bern, Inselspital, Bern, Switzerland.
33
School of Psychology and Counselling and IHBI, Queensland University of Technology, Brisbane, Australia.
34
Centre for Age-Related Medicine (SESAM), Stavanger University Hospital, Stavanger, Norway.
35
Wolfson Centre for Age-Related Diseases, King's College London, London, United Kingdom.

Abstract

BACKGROUND:

Striatal dopamine deficiency and metabolic changes are well-known phenomena in dementia with Lewy bodies and can be quantified in vivo by 123 I-Ioflupane brain single-photon emission computed tomography of dopamine transporter and 18 F-fluorodesoxyglucose PET. However, the linkage between both biomarkers is ill-understood.

OBJECTIVE:

We used the hitherto largest study cohort of combined imaging from the European consortium to elucidate the role of both biomarkers in the pathophysiological course of dementia with Lewy bodies.

METHODS:

We compared striatal dopamine deficiency and glucose metabolism of 84 dementia with Lewy body patients and comparable healthy controls. After normalization of data, we tested their correlation by region-of-interest-based and voxel-based methods, controlled for study center, age, sex, education, and current cognitive impairment. Metabolic connectivity was analyzed by inter-region coefficients stratified by dopamine deficiency and compared to healthy controls.

RESULTS:

There was an inverse relationship between striatal dopamine availability and relative glucose hypermetabolism, pronounced in the basal ganglia and in limbic regions. With increasing dopamine deficiency, metabolic connectivity showed strong deteriorations in distinct brain regions implicated in disease symptoms, with greatest disruptions in the basal ganglia and limbic system, coincident with the pattern of relative hypermetabolism.

CONCLUSIONS:

Relative glucose hypermetabolism and disturbed metabolic connectivity of limbic and basal ganglia circuits are metabolic correlates of dopamine deficiency in dementia with Lewy bodies. Identification of specific metabolic network alterations in patients with early dopamine deficiency may serve as an additional supporting biomarker for timely diagnosis of dementia with Lewy bodies. © 2019 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.

KEYWORDS:

Lewy body dementia; PET imaging; dopamine deficiency; glucose metabolism; metabolic connectivity

PMID:
31840326
DOI:
10.1002/mds.27945
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