Parkinson patients have a presynaptic serotonergic deficit: A dynamic deep brain stimulation PET study
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Parkinson patients have a presynaptic serotonergic deficit : A dynamic deep brain stimulation PET study. / Jørgensen, Louise M; Henriksen, Tove; Mardosiene, Skirmante; Keller, Sune H.; Stenbæk, Dea S; Hansen, Hanne D.; Jespersen, Bo; Thomsen, Carsten; Weikop, Pia; Svarer, Claus; Knudsen, Gitte M.
In: Journal of Cerebral Blood Flow and Metabolism, Vol. 41, No. 8, 2021, p. 1954-1963.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Parkinson patients have a presynaptic serotonergic deficit
T2 - A dynamic deep brain stimulation PET study
AU - Jørgensen, Louise M
AU - Henriksen, Tove
AU - Mardosiene, Skirmante
AU - Keller, Sune H.
AU - Stenbæk, Dea S
AU - Hansen, Hanne D.
AU - Jespersen, Bo
AU - Thomsen, Carsten
AU - Weikop, Pia
AU - Svarer, Claus
AU - Knudsen, Gitte M
PY - 2021
Y1 - 2021
N2 - Patients with Parkinson's disease (PD) often suffer from non-motor symptoms, which may be caused by serotonergic dysfunction. Apart from alleviating the motor symptoms, Deep Brain Stimulation (DBS) in the subthalamic nucleus (STN) may also influence non-motor symptoms. The aim of this study is to investigate how turning DBS off affects the serotonergic system. We here exploit a novel functional PET neuroimaging methodology to evaluate the preservation of serotonergic neurons and capacity to release serotonin. We measured cerebral 5-HT1BR binding in 13 DBS-STN treated PD patients, at baseline and after turning DBS off. Ten age-matched volunteers served as controls. Clinical measures of motor symptoms were assessed under the two conditions and correlated to the PET measures of the static and dynamic integrity of the serotonergic system. PD patients exhibited a significant loss of frontal and parietal 5-HT1BR, and the loss was significantly correlated to motor symptom severity. We saw a corresponding release of serotonin, but only in brain regions with preserved 5-HT1BR, suggesting the presence of a presynaptic serotonergic deficit. Our study demonstrates that DBS-STN dynamically regulates the serotonin system in PD, and that preservation of serotonergic functions may be predictive of DBS-STN effects.
AB - Patients with Parkinson's disease (PD) often suffer from non-motor symptoms, which may be caused by serotonergic dysfunction. Apart from alleviating the motor symptoms, Deep Brain Stimulation (DBS) in the subthalamic nucleus (STN) may also influence non-motor symptoms. The aim of this study is to investigate how turning DBS off affects the serotonergic system. We here exploit a novel functional PET neuroimaging methodology to evaluate the preservation of serotonergic neurons and capacity to release serotonin. We measured cerebral 5-HT1BR binding in 13 DBS-STN treated PD patients, at baseline and after turning DBS off. Ten age-matched volunteers served as controls. Clinical measures of motor symptoms were assessed under the two conditions and correlated to the PET measures of the static and dynamic integrity of the serotonergic system. PD patients exhibited a significant loss of frontal and parietal 5-HT1BR, and the loss was significantly correlated to motor symptom severity. We saw a corresponding release of serotonin, but only in brain regions with preserved 5-HT1BR, suggesting the presence of a presynaptic serotonergic deficit. Our study demonstrates that DBS-STN dynamically regulates the serotonin system in PD, and that preservation of serotonergic functions may be predictive of DBS-STN effects.
U2 - 10.1177/0271678X20982389
DO - 10.1177/0271678X20982389
M3 - Journal article
C2 - 33461410
VL - 41
SP - 1954
EP - 1963
JO - Journal of Cerebral Blood Flow and Metabolism
JF - Journal of Cerebral Blood Flow and Metabolism
SN - 0271-678X
IS - 8
ER -
ID: 255685974