The chronic use of serotonin norepinephrine reuptake inhibitors facilitates dyskinesia priming in early Parkinson's disease.

Depression Levodopa-induced dyskinesias Locus coeruleus Motor fluctuations Noradrenaline Serotonin

Journal

Journal of neurology
ISSN: 1432-1459
Titre abrégé: J Neurol
Pays: Germany
ID NLM: 0423161

Informations de publication

Date de publication:
08 May 2024
Historique:
received: 03 02 2024
accepted: 24 04 2024
revised: 12 04 2024
medline: 9 5 2024
pubmed: 9 5 2024
entrez: 8 5 2024
Statut: aheadofprint

Résumé

Parkinson's disease (PD) patients are frequently exposed to antidepressant medications (ADMs). Norepinephrine (NE) and serotonin (5HT) systems have a role in levodopa-induced dyskinesias (LID) pathophysiology. We performed a longitudinal analysis on the PPMI cohort including drug-naïve PD patients, who are progressively exposed to dopamine replacement therapies (DRTs) to test the effect of ADM exposure on LID development by the 4th year of follow-up. LID prevalence (according to MDS UPDRS score 4.1 ≥ 1) was 16% (42/251); these patients were more likely women (p = 0.01), had higher motor (p < 0.001) and depression scores (p = 0.01) and lower putaminal DAT binding ratio (p = 0.01). LID were associated with the exposure time to L-DOPA (2.2 ± 1.07 vs 2.6 ± 0.9, p = 0.02) and to the exposure to ADMs, in particular to SNRI (4.8% vs 21.4%, p < 0.001). The latter persisted after correcting for significant covariates (e.g., disease duration, cognitive status, motor impairment, depression, dopaminergic denervation). A similar difference in LID prevalence in PD patients exposed vs non-exposed to SNRI was observed on matched data by the real-world TriNetX repository (22% vs 13%, p < 0.001). This study supports the presence of an effect of SNRI on LID priming in patients with early PD. Independent prospective cohort studies are warranted to further verify such association.

Sections du résumé

BACKGROUND BACKGROUND
Parkinson's disease (PD) patients are frequently exposed to antidepressant medications (ADMs). Norepinephrine (NE) and serotonin (5HT) systems have a role in levodopa-induced dyskinesias (LID) pathophysiology.
METHODS METHODS
We performed a longitudinal analysis on the PPMI cohort including drug-naïve PD patients, who are progressively exposed to dopamine replacement therapies (DRTs) to test the effect of ADM exposure on LID development by the 4th year of follow-up.
RESULTS RESULTS
LID prevalence (according to MDS UPDRS score 4.1 ≥ 1) was 16% (42/251); these patients were more likely women (p = 0.01), had higher motor (p < 0.001) and depression scores (p = 0.01) and lower putaminal DAT binding ratio (p = 0.01). LID were associated with the exposure time to L-DOPA (2.2 ± 1.07 vs 2.6 ± 0.9, p = 0.02) and to the exposure to ADMs, in particular to SNRI (4.8% vs 21.4%, p < 0.001). The latter persisted after correcting for significant covariates (e.g., disease duration, cognitive status, motor impairment, depression, dopaminergic denervation). A similar difference in LID prevalence in PD patients exposed vs non-exposed to SNRI was observed on matched data by the real-world TriNetX repository (22% vs 13%, p < 0.001).
DISCUSSION CONCLUSIONS
This study supports the presence of an effect of SNRI on LID priming in patients with early PD. Independent prospective cohort studies are warranted to further verify such association.

Identifiants

pubmed: 38720139
doi: 10.1007/s00415-024-12400-6
pii: 10.1007/s00415-024-12400-6
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

© 2024. Springer-Verlag GmbH Germany, part of Springer Nature.

Références

Bloem BR, Okun MS, Klein C (2021) Parkinson’s disease. Lancet 397:2284–2303. https://doi.org/10.1016/S0140-6736(21)00218-X
doi: 10.1016/S0140-6736(21)00218-X pubmed: 33848468
Rodriguez-Blazquez C, Schrag A, Rizos A, Chaudhuri KR, Martinez-Martin P, Weintraub D (2020) Prevalence of non-motor symptoms and non-motor fluctuations in Parkinson’s disease using the MDS-NMS. Mov Disord Clin Pract 8:231–239. https://doi.org/10.1002/mdc3.13122
doi: 10.1002/mdc3.13122 pubmed: 33553493 pmcid: 7853195
Seppi K, Ray Chaudhuri K, Coelho M, Fox SH, Katzenschlager R, Perez Lloret S, Weintraub D, Sampaio C, the collaborators of the Parkinson’s Disease Update on Non-Motor Symptoms Study Group on behalf of the Movement Disorders Society Evidence-Based Medicine Committee (2019) Update on treatments for nonmotor symptoms of Parkinson’s disease-an evidence-based medicine review. Mov Disord 34:180–198. https://doi.org/10.1002/mds.27602
doi: 10.1002/mds.27602 pubmed: 30653247 pmcid: 6916382
Krøigård T, Christensen J, Wermuth L, Ritz B, Lassen CF (2014) The use of antidepressant medication in Parkinson’s disease patients is not affected by the type of antiparkinson medication. J Parkinsons Dis 4:327–330. https://doi.org/10.3233/JPD-140386
doi: 10.3233/JPD-140386 pubmed: 24919822
Carta M, Carlsson T, Kirik D, Björklund A (2007) Dopamine released from 5-HT terminals is the cause of L-DOPA-induced dyskinesia in parkinsonian rats. Brain 130:1819–1833. https://doi.org/10.1093/brain/awm082
doi: 10.1093/brain/awm082 pubmed: 17452372
Carta M, Björklund A (2018) The serotonergic system in L-DOPA-induced dyskinesia: pre-clinical evidence and clinical perspective. J Neural Transm (Vienna) 125:1195–1202. https://doi.org/10.1007/s00702-018-1865-5
doi: 10.1007/s00702-018-1865-5 pubmed: 29480391
Cenci MA, Lundblad M (2006) Post- versus presynaptic plasticity in L-DOPA-induced dyskinesia. J Neurochem 99:381–392. https://doi.org/10.1111/j.1471-4159.2006.04124.x
doi: 10.1111/j.1471-4159.2006.04124.x pubmed: 16942598
Chase TN (1998) Levodopa therapy: consequences of the nonphysiologic replacement of dopamine. Neurology 50:S17-25. https://doi.org/10.1212/wnl.50.5_suppl_5.s17
doi: 10.1212/wnl.50.5_suppl_5.s17 pubmed: 9591518
Arai A, Tomiyama M, Kannari K, Kimura T, Suzuki C, Watanabe M, Kawarabayashi T, Shen H, Shoji M (2008) Reuptake of L-DOPA-derived extracellular DA in the striatum of a rodent model of Parkinson’s disease via norepinephrine transporter. Synapse 62:632–635. https://doi.org/10.1002/syn.20535
doi: 10.1002/syn.20535 pubmed: 18509855
Munoz A, Li Q, Gardoni F, Marcello E, Qin C, Carls-son T et al (2008) Combined 5-HT1A and 5-HT1B receptor agonists for the treatment of L-DOPA-induced dyskinesia. Brain 131:3380–3394
doi: 10.1093/brain/awn235 pubmed: 18952677
Ostock CY, Lindenbach D, Goldenberg AA, Kampton E, Bishop C (2014) Effects of noradrenergic denervation by anti-DBH-saporin on behavioral responsivity to L-DOPA in the hemi-parkinsonian rat. Behav Brain Res 270:75–85. https://doi.org/10.1016/j.bbr.2014.05.009
doi: 10.1016/j.bbr.2014.05.009 pubmed: 24837745 pmcid: 4103008
Shin E, Rogers JT, Devoto P, Björklund A, Carta M (2014) Noradrenaline neuron degeneration contributes to motor impairments and development of L-DOPA-induced dyskinesia in a rat model of Parkinson’s disease. Exp Neurol 257:25–38. https://doi.org/10.1016/j.expneurol.2014.04.011
doi: 10.1016/j.expneurol.2014.04.011 pubmed: 24747357
Mazzucchi S, Frosini D, Ripoli A, Nicoletti V, Linsalata G, Bonuccelli U, Ceravolo R (2015) Serotonergic antidepressant drugs and L-dopa-induced dyskinesias in Parkinson’s disease. Acta Neurol Scand 131:191–195. https://doi.org/10.1111/ane.12314
doi: 10.1111/ane.12314 pubmed: 25274076
Bezard E, Tronci E, Pioli EY, Li Q, Porras G, Björklund A, Carta M (2013) Study of the antidyskinetic effect of eltoprazine in animal models of levodopa-induced dyskinesia. Mov Disord 28:1088–1096. https://doi.org/10.1002/mds.25366
doi: 10.1002/mds.25366 pubmed: 23389842
Tronci E, Fidalgo C, Stancampiano R, Carta M (2015) Effect of selective and non-selective serotonin receptor activation on L-DOPA-induced therapeutic efficacy and dyskinesia in parkinsonian rats. Behav Brain Res 292:300–294. https://doi.org/10.1016/j.bbr.2015.06.034
doi: 10.1016/j.bbr.2015.06.034 pubmed: 26119238
Eskow KL, Gupta V, Alam S, Park JY, Bishop C (2007) The partial 5-HT(1A) agonist buspirone reduces the expression and development of l-DOPA-induced dyskinesia in rats and improves l-DOPA efficacy. Pharmacol Biochem Behav 87:306–314. https://doi.org/10.1016/j.pbb.2007.05.002
doi: 10.1016/j.pbb.2007.05.002 pubmed: 17553556
Politis M, Wu K, Loane C, Brooks DJ, Kiferle L, Turkheimer FE, Bain P, Molloy S, Piccini P (2014) Serotonergic mechanisms responsible for levodopa-induced dyskinesias in Parkinson’s disease patients. J Clin Invest 124:1340–1349. https://doi.org/10.1172/JCI71640
doi: 10.1172/JCI71640 pubmed: 24531549 pmcid: 3934188
Fidalgo C, Ko WK, Tronci E, Li Q, Stancampiano R, Chuan Q, Bezard E, Carta M (2015) Effect of serotonin transporter blockade on L-DOPA-induced dyskinesia in animal models of Parkinson’s disease. Neuroscience 298:389–396. https://doi.org/10.1016/j.neuroscience.2015.04.027
doi: 10.1016/j.neuroscience.2015.04.027 pubmed: 25907446
Szabo ST, de Montigny C, Blier P (2000) Progressive attenuation of the firing activity of locus coeruleus noradrenergic neurons by sustained administration of selective serotonin reuptake inhibitors. Int J Neuropsychopharmacol 3:1–11
doi: 10.1017/S1461145700001772 pubmed: 11343573
Ostock CY, Bhide N, Goldenberg AA, George JA, Bishop C (2018) Striatal norepinephrine efflux in l-DOPA-induced dyskinesia. Neurochem Int 114:85–98. https://doi.org/10.1016/j.neuint.2018.01.010
doi: 10.1016/j.neuint.2018.01.010 pubmed: 29371053
Chotibut T, Apple DM, Jefferis R, Salvatore MF (2012) Dopamine transporter loss in 6-OHDA Parkinson’s model is unmet by parallel reduction in dopamine uptake. PLoS ONE 7:e52322. https://doi.org/10.1371/journal.pone.0052322
doi: 10.1371/journal.pone.0052322 pubmed: 23300642 pmcid: 3530604
Morón JA, Brockington A, Wise RA, Rocha BA, Hope BT (2002) Dopamine uptake through the norepinephrine transporter in brain regions with low levels of the dopamine transporter: evidence from knock-out mouse lines. J Neurosci 22:389–395. https://doi.org/10.1523/JNEUROSCI.22-02-00389.2002.PMC6758674
doi: 10.1523/JNEUROSCI.22-02-00389.2002.PMC6758674 pubmed: 11784783 pmcid: 6758674
Chotibut T, Fields V, Salvatore MF (2014) Norepinephrine transporter inhibition with desipramine exacerbates L-DOPA-induced dyskinesia: role for synaptic dopamine regulation in denervated nigrostriatal terminals. Mol Pharmacol 86:675–685. https://doi.org/10.1124/mol.114.093302
doi: 10.1124/mol.114.093302 pubmed: 25208966
Fulceri F, Biagioni F, Ferrucci M, Lazzeri G, Bartalucci A, Galli V, Ruggieri S, Paparelli A, Fornai F (2007) Abnormal involuntary movements (AIMs) following pulsatile dopaminergic stimulation: severe deterioration and morphological correlates following the loss of locus coeruleus neurons. Brain Res 1135:219–229. https://doi.org/10.1016/j.brainres.2006.12.030
doi: 10.1016/j.brainres.2006.12.030 pubmed: 17222394
Czubak A, Nowakowska E, Golembiowska K, Kus K, Burda K, Metelska J (2010) Effect of venlafaxine and nicotine on the level of neurotransmitters and their metabolites in rat brains. J Physiol Pharmacol 61:339–346
pubmed: 20610865
Barnum CJ, Bhide N, Lindenbach D, Surrena MA, Goldenberg AA, Tignor S, Klioueva A, Walters H, Bishop C (2012) Effects of noradrenergic denervation on L-DOPA-induced dyskinesia and its treatment by α- and β-adrenergic receptor antagonists in hemiparkinsonian rats. Pharmacol Biochem Behav 100:607–615. https://doi.org/10.1016/j.pbb.2011.09.009
doi: 10.1016/j.pbb.2011.09.009 pubmed: 21978941
Holmberg M, Scheinin M, Kurose H, Miettinen R (1999) Adrenergic alpha2C-receptors reside in rat striatal GABAergic projection neurons: comparison of radioligand binding and immunohistochemistry. Neuroscience 93:1323–1333. https://doi.org/10.1016/s0306-4522(99)00260-2
doi: 10.1016/s0306-4522(99)00260-2 pubmed: 10501456
Hara M, Fukui R, Hieda E, Kuroiwa M, Bateup HS, Kano T, Greengard P, Nishi A (2010) Role of adrenoceptors in the regulation of dopamine/DARPP-32 signaling in neostriatal neurons. J Neurochem 113:1046–1059. https://doi.org/10.1111/j.1471-4159.2010.06668.x
doi: 10.1111/j.1471-4159.2010.06668.x pubmed: 20236221 pmcid: 2861145
Miguelez C, Aristieta A, Cenci MA, Ugedo L (2011) The locus coeruleus is directly implicated in L-DOPA-induced dyskinesia in parkinsonian rats: an electrophysiological and behavioural study. PLoS ONE 6(9):e24679. https://doi.org/10.1371/journal.pone.0024679
doi: 10.1371/journal.pone.0024679 pubmed: 21931808 pmcid: 3170382
Eusebi P, Romoli M, Paoletti FP, Tambasco N, Calabresi P, Parnetti L (2018) Risk factors of levodopa-induced dyskinesia in Parkinson’s disease: results from the PPMI cohort. NPJ Parkinsons Dis 4:33. https://doi.org/10.1038/s41531-018-0069-x
doi: 10.1038/s41531-018-0069-x pubmed: 30480086 pmcid: 6240081

Auteurs

Massimo Marano (M)

Neurology, Neurophysiology, Neurobiology and Psychiatry Unit, Department of Medicine, Università Campus Bio-Medico di Roma, Via Alvaro del Portillo 200, 00128, Rome, Italy. m.marano@policlinicocampus.it.
Fondazione Policlinico Universitario Campus Bio-Medico, Viale Alvaro del Portillo 200, 00128, Rome, Italy. m.marano@policlinicocampus.it.

Andrea Pilotto (A)

Neurology Unit, Department of Clinical and Experimental Sciences, University of Brescia, Brescia, Italy.
Laboratory of Digital Neurology and Biosensors, University of Brescia, Brescia, Italy.
Neurology Unit, Department of Continuity of Care and Frailty, ASST Spedali Civili Brescia Hospital, Brescia, Italy.
Brain Health Center, University of Brescia, Brescia, Italy.

Alessandro Padovani (A)

Neurology Unit, Department of Clinical and Experimental Sciences, University of Brescia, Brescia, Italy.
Laboratory of Digital Neurology and Biosensors, University of Brescia, Brescia, Italy.
Neurology Unit, Department of Continuity of Care and Frailty, ASST Spedali Civili Brescia Hospital, Brescia, Italy.
Brain Health Center, University of Brescia, Brescia, Italy.

Deepak Gupta (D)

Department of Neurological Sciences, Larner College of Medicine, University of Vermont, Burlington, VT, USA.

Giorgio Vivacqua (G)

Laboratory of Microscopic and Ultrastructural Anatomy, Università Campus Bio-Medico di Roma, Via Alvaro del Portillo 21, 00128, Roma, Italy.

Alessandro Magliozzi (A)

Neurology, Neurophysiology, Neurobiology and Psychiatry Unit, Department of Medicine, Università Campus Bio-Medico di Roma, Via Alvaro del Portillo 200, 00128, Rome, Italy.
Fondazione Policlinico Universitario Campus Bio-Medico, Viale Alvaro del Portillo 200, 00128, Rome, Italy.

Vincenzo Di Lazzaro (V)

Neurology, Neurophysiology, Neurobiology and Psychiatry Unit, Department of Medicine, Università Campus Bio-Medico di Roma, Via Alvaro del Portillo 200, 00128, Rome, Italy.
Fondazione Policlinico Universitario Campus Bio-Medico, Viale Alvaro del Portillo 200, 00128, Rome, Italy.

Manolo Carta (M)

Department of Biomedical Sciences, University of Cagliari, Cagliari, CA, Italy.

Mario Meloni (M)

Neurology Unit, Azienda Ospedaliera Universitaria di Cagliari, Cagliari, Italy.

Classifications MeSH