Altered sensorimotor cortex noradrenergic function in idiopathic REM sleep behaviour disorder: A PET study

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Altered sensorimotor cortex noradrenergic function in idiopathic REM sleep behaviour disorder : A PET study. / Andersen, Katrine B.; Hansen, Allan K.; Sommerauer, Michael; Fedorova, Tatyana D.; Knudsen, Karoline; Vang, Kim; Van Den Berge, Nathalie; Kinnerup, Martin; Nahimi, Adjmal; Pavese, Nicola; Brooks, David J.; Borghammer, Per.

In: Parkinsonism & Related Disorders, Vol. 75, 06.2020, p. 63-69.

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@article{cfd681ddc7cd4450a9a6f5cb7936464f,
title = "Altered sensorimotor cortex noradrenergic function in idiopathic REM sleep behaviour disorder: A PET study",
abstract = "Introduction: Noradrenergic denervation is thought to aggravate motor dysfunction in Parkinson's disease (PD). In a previous PET study with the norepinephrine transporter (NART) ligand C-11-MeNER, we detected reduced NART binding in primary sensorimotor cortex (M1S1) of PD patients. Idiopathic rapid-eye-movement sleep behaviour disorder (iRBD) is a phenotype of prodromal PD. Using C-11-MeNER PET, we investigated whether iRBD patients showed similar NART binding reductions in M1S1 cortex as PD patients. Additionally, we investigated whether C-11-MeNER binding and loss of nigrostriatal dopamine storage capacity measured with F-18-DOPA PET were correlated.Methods: 17 iRBD patients, 16 PD patients with (PDRBD+) and 14 without RBD (PDRBD-), and 25 control subjects underwent C-11-MeNER PET. iRBD patients also had F-18-DOPA PET. Volume-of-interest analyses and voxel-level statistical parametric mapping were performed.Results: Partial-volume corrected C-11-MeNER binding potential (BPND) values in M1S1 differed across the groups (P = 0.022) with the iRBD and PDRBD+ groups showing significant reductions (controls vs. iRBD P = 0.007; control vs. PDRBD+ P = 0.008). Voxel-wise comparisons confirmed reductions of M1S1 C-11-MeNER binding in PD and iRBD patients. Significant correlation was seen between putaminal F-18-DOPA uptake and thalamic C-11-MeNER binding in iRBD patients (r(2) = 0.343, P = 0.013).Conclusions: This study found altered noradrenergic neurotransmission in the M1S1 cortex of iRBD patients. The observed reduction of M1S1 C-11-MeNER binding in iRBD may represent noradrenergic terminal degeneration or physiological down-regulation of NARTs in this prodromal phenotype of PD. The correlation between thalamic C-11-MeNER binding and putaminal F-18-DOPA binding suggests that these neurotransmitter systems degenerate in parallel in the iRBD phenotype of prodromal PD.",
keywords = "C-MeNER positron emission tomography (PET), Idiopathic rapid-eye-movement (REM) sleep behaviour disorder (RBD), Motor cortex, Noradrenaline, Parkinson's disease, Primary motor-sensory cortex",
author = "Andersen, {Katrine B.} and Hansen, {Allan K.} and Michael Sommerauer and Fedorova, {Tatyana D.} and Karoline Knudsen and Kim Vang and {Van Den Berge}, Nathalie and Martin Kinnerup and Adjmal Nahimi and Nicola Pavese and Brooks, {David J.} and Per Borghammer",
year = "2020",
month = jun,
doi = "10.1016/j.parkreldis.2020.05.013",
language = "English",
volume = "75",
pages = "63--69",
journal = "Parkinsonism & Related Disorders",
issn = "1353-8020",
publisher = "Elsevier Ltd",

}

RIS

TY - JOUR

T1 - Altered sensorimotor cortex noradrenergic function in idiopathic REM sleep behaviour disorder

T2 - A PET study

AU - Andersen, Katrine B.

AU - Hansen, Allan K.

AU - Sommerauer, Michael

AU - Fedorova, Tatyana D.

AU - Knudsen, Karoline

AU - Vang, Kim

AU - Van Den Berge, Nathalie

AU - Kinnerup, Martin

AU - Nahimi, Adjmal

AU - Pavese, Nicola

AU - Brooks, David J.

AU - Borghammer, Per

PY - 2020/6

Y1 - 2020/6

N2 - Introduction: Noradrenergic denervation is thought to aggravate motor dysfunction in Parkinson's disease (PD). In a previous PET study with the norepinephrine transporter (NART) ligand C-11-MeNER, we detected reduced NART binding in primary sensorimotor cortex (M1S1) of PD patients. Idiopathic rapid-eye-movement sleep behaviour disorder (iRBD) is a phenotype of prodromal PD. Using C-11-MeNER PET, we investigated whether iRBD patients showed similar NART binding reductions in M1S1 cortex as PD patients. Additionally, we investigated whether C-11-MeNER binding and loss of nigrostriatal dopamine storage capacity measured with F-18-DOPA PET were correlated.Methods: 17 iRBD patients, 16 PD patients with (PDRBD+) and 14 without RBD (PDRBD-), and 25 control subjects underwent C-11-MeNER PET. iRBD patients also had F-18-DOPA PET. Volume-of-interest analyses and voxel-level statistical parametric mapping were performed.Results: Partial-volume corrected C-11-MeNER binding potential (BPND) values in M1S1 differed across the groups (P = 0.022) with the iRBD and PDRBD+ groups showing significant reductions (controls vs. iRBD P = 0.007; control vs. PDRBD+ P = 0.008). Voxel-wise comparisons confirmed reductions of M1S1 C-11-MeNER binding in PD and iRBD patients. Significant correlation was seen between putaminal F-18-DOPA uptake and thalamic C-11-MeNER binding in iRBD patients (r(2) = 0.343, P = 0.013).Conclusions: This study found altered noradrenergic neurotransmission in the M1S1 cortex of iRBD patients. The observed reduction of M1S1 C-11-MeNER binding in iRBD may represent noradrenergic terminal degeneration or physiological down-regulation of NARTs in this prodromal phenotype of PD. The correlation between thalamic C-11-MeNER binding and putaminal F-18-DOPA binding suggests that these neurotransmitter systems degenerate in parallel in the iRBD phenotype of prodromal PD.

AB - Introduction: Noradrenergic denervation is thought to aggravate motor dysfunction in Parkinson's disease (PD). In a previous PET study with the norepinephrine transporter (NART) ligand C-11-MeNER, we detected reduced NART binding in primary sensorimotor cortex (M1S1) of PD patients. Idiopathic rapid-eye-movement sleep behaviour disorder (iRBD) is a phenotype of prodromal PD. Using C-11-MeNER PET, we investigated whether iRBD patients showed similar NART binding reductions in M1S1 cortex as PD patients. Additionally, we investigated whether C-11-MeNER binding and loss of nigrostriatal dopamine storage capacity measured with F-18-DOPA PET were correlated.Methods: 17 iRBD patients, 16 PD patients with (PDRBD+) and 14 without RBD (PDRBD-), and 25 control subjects underwent C-11-MeNER PET. iRBD patients also had F-18-DOPA PET. Volume-of-interest analyses and voxel-level statistical parametric mapping were performed.Results: Partial-volume corrected C-11-MeNER binding potential (BPND) values in M1S1 differed across the groups (P = 0.022) with the iRBD and PDRBD+ groups showing significant reductions (controls vs. iRBD P = 0.007; control vs. PDRBD+ P = 0.008). Voxel-wise comparisons confirmed reductions of M1S1 C-11-MeNER binding in PD and iRBD patients. Significant correlation was seen between putaminal F-18-DOPA uptake and thalamic C-11-MeNER binding in iRBD patients (r(2) = 0.343, P = 0.013).Conclusions: This study found altered noradrenergic neurotransmission in the M1S1 cortex of iRBD patients. The observed reduction of M1S1 C-11-MeNER binding in iRBD may represent noradrenergic terminal degeneration or physiological down-regulation of NARTs in this prodromal phenotype of PD. The correlation between thalamic C-11-MeNER binding and putaminal F-18-DOPA binding suggests that these neurotransmitter systems degenerate in parallel in the iRBD phenotype of prodromal PD.

KW - C-MeNER positron emission tomography (PET)

KW - Idiopathic rapid-eye-movement (REM) sleep behaviour disorder (RBD)

KW - Motor cortex

KW - Noradrenaline

KW - Parkinson's disease

KW - Primary motor-sensory cortex

UR - http://www.scopus.com/inward/record.url?scp=85085354265&partnerID=8YFLogxK

U2 - 10.1016/j.parkreldis.2020.05.013

DO - 10.1016/j.parkreldis.2020.05.013

M3 - Journal article

C2 - 32480309

AN - SCOPUS:85085354265

VL - 75

SP - 63

EP - 69

JO - Parkinsonism & Related Disorders

JF - Parkinsonism & Related Disorders

SN - 1353-8020

ER -