Monoamine Reuptake Inhibitors in Parkinson’s Disease

Huot, Philippe; Fox, Susan H.; Brotchie, Jonathan M.

doi:10.1155/2015/609428

Cited by 26 publications

(24 citation statements)

References 603 publications

(556 reference statements)

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“…Blockade of overactive 5HT 2c receptor-mediated activity with selective 5HT 2c receptor antagonists as agomelatine can potentiate the antiparkinsonian action of dopamine receptor agonists. 22 This would explain the improvement observed in our study not only of the parkinsonian symptoms of PD patients with depression treated with agomelatine, but also of the index of PLM mediated by the dopaminergic system too.…”

Section: Discussionsupporting

confidence: 55%

Agomelatine for Depression in Parkinson Disease

Ávila¹,

Cardona²,

Martı́n-Baranera³

et al. 2015

Journal of Clinical Psychopharmacology

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Depression and sleep disorders are among the most prevalent nonmotor symptoms of Parkinson disease (PD). Because agomelatine acts as a MT1 and MT2 agonist and as a 5HT2c antagonist, this study was designed to assess the efficacy of agomelatine in treating depressive symptoms in PD patients, and the potential changes both in sleep quality and motor symptoms. Depressed patients with PD were treated with agomelatine for 6 months, and they were evaluated with an array of scales. Completed nocturnal video-polysomnography was performed at baseline and week 12. The efficacy analysis population included 24 patients (12 men). The mean (SD) age was 75.2 (8.3) years. The mean (SD) daily dose of agomelatine was 25.00 (10.43) mg at 24 weeks. No changes in dopamine replacement therapy were made. There was a significant decrease in the 17-item Hamilton Depression Scale score over the course of the study (P < 0.0005). The Scales for Outcomes in Parkinson disease Sleep Questionnaire showed a statistically significant improvement over time in each of its subscales: nighttime sleep (P < 0.005), last month nighttime sleep (P < 0.0005), and daytime sleepiness (P < 0.0005). Surprisingly, changes over time in the motor subscale of Unified Parkinson Disease Rating Scale were statistically significant (P < 0.0005). Periodic limb movements and awakenings measured by polysomnography improved significantly (P < 0.005 and P < 0.05, respectively). We concluded that the use of agomelatine in PD depressed patients may have a considerable therapeutic potential because of its dual action for treating both symptoms of depression and disturbed sleep given its secondary beneficial effects regarding the reduction of extrapyramidal symptoms.

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Section: Discussionsupporting

confidence: 55%

Agomelatine for Depression in Parkinson Disease

Ávila¹,

Cardona²,

Martı́n-Baranera³

et al. 2015

Journal of Clinical Psychopharmacology

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“…Brasofensine, bupropion, methylphenidate, and nomifensine are dual DAT and NAT inhibitors (with a DAT/NAT ratio between 0.5 and 4; Huot et al, 2015) and have been studied as potential therapies for PD.…”

Section: Dual Dat and Nat Inhibitorsmentioning

confidence: 99%

“…These theoretical antiparkinsonian benefits form the rationale underlying the potential use of DAT inhibitors in PD. Many DAT inhibitors have been identified and span a spectrum of selectivity for DAT over other monoamine transporters; the pharmacology of these was recently reviewed in detail elsewhere (Huot et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

“…Throughout, we divide the monoamine reuptake inhibitors based on their affinity for DATs, noradrenaline transporters (NATs), and serotonin transporters (SERTs). As in a previous article (Huot et al, 2015), we considered that a compound was selective for a transporter when its affinity for that transporter was greater than 10-fold its affinity for that of the other transporters.…”

Section: Introductionmentioning

confidence: 99%

“…Selective DAT Inhibitors 909 (vanoxerine;[1][2]methoxy] ethyl]-4-(3-phenylpropyl)piperazine dihydrochloride) and SEP-228,791 are selective DAT inhibitors (Huot et al, 2015) that have been evaluated in the MPTP-lesioned monkey. To date, neither GBR-12,909 nor SEP-228,791 has been studied in idiopathic PD.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Dopamine Reuptake Inhibitors in Parkinsons Disease: A Review of Nonhuman Primate Studies and Clinical Trials

Fox

Brotchie

2016

Journal of Pharmacology and Experimental Therapeutics

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Striatal dopamine deficiency is the core feature of the pathology of Parkinson's disease (PD), and dopamine replacement with L-3,4-dihydroxyphenylalanine (L-DOPA) is the mainstay of PD treatment. Unfortunately, chronic L-DOPA administration is marred by the emergence of dyskinesia and wearing-off. Alternatives to L-DOPA for alleviation of parkinsonism are of interest, although none can match the efficacy of L-DOPA to date. Catechol-O-methyltransferase and monoamine oxidase inhibitors are currently used to alleviate wearing-off, but they do not increase "on-time" without exacerbating dyskinesia. Alternate approaches to dopamine replacement in parkinsonism generally (and to wearing-off and dyskinesia, specifically) are therefore urgently needed. Inasmuch as they increase synaptic dopamine levels, dopamine transporter (DAT) inhibitors, whether they are selective or have actions on noradrenaline or serotonin transporters, theoretically represent an attractive way to alleviate parkinsonism per se and potentially enhance L-DOPA antiparkinsonian action (provided that sufficient dopamine terminals remain within the striatum). Several nonhuman primate studies and clinical trials have been performed to evaluate the potential of DAT inhibitors for PD. In this article, we review nonhuman primate studies and clinical trials, we summarize the current knowledge of DAT inhibitors in PD, and we propose a hypothesis as to how tailoring the selectivity of DAT inhibitors might maximize the benefits of DAT inhibition in PD.

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A simple and sensitive high‐performance liquid chromatography–electrochemical detection assay for the quantitative determination of monoamines and respective metabolites in six discrete brain regions of mice

Allen

Rednour

Shepard

et al. 2017

Biomedical Chromatography

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A rapid, sensitive, and reproducible assay is described for the quantitative determination of the monoamine neurotransmitters dopamine, norepinephrine and serotonin, their metabolites, and the internal standard 3,4-dihydroxybenzlyamine hydro-bromide in mouse brain homogenate using high-performance liquid chromatography with electrochemical detection. The method was validated in the following brain areas: frontal cortex, striatum, nucleus accumbens, hippocampus, substantia nigra pars compacta and ventral tegmental area. Biogenic amines and relevant metabolites were extracted from discrete brain regions using a simple protein precipitation procedure, and the chromatography was achieved using a C column. The method was accurate over the linear range of 0.300-30 ng/mL (r = 0.999) for dopamine and 0.300-15 ng/mL (r = 0.999) for norepinephrine, 3,4-dihydroxybenzlyamine hydro-bromide, homovanillic acid and 5-hydroxyindolacetic acid, with detection limits of ~0.125 ng/mL (5 pg on column) for each of these analytes. Accuracy and linearity for serotonin were observed throughout the concentration range of 0.625-30 ng/mL (r = 0.998) with an analytical detection limit of ~0.300 ng/mL (12 pg on column). Relative recoveries for all analytes were approximately ≥90% and the analytical run time was <10 min. The described method utilized minimal sample preparation procedures and was optimized to provide the sensitivity limits required for simultaneous monoamine and metabolite analysis in small, discrete brain tissue samples.

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Monoamine Reuptake Inhibitors in Parkinson’s Disease

Cited by 26 publications

References 603 publications

Agomelatine for Depression in Parkinson Disease

Agomelatine for Depression in Parkinson Disease

Dopamine Reuptake Inhibitors in Parkinsons Disease: A Review of Nonhuman Primate Studies and Clinical Trials

A simple and sensitive high‐performance liquid chromatography–electrochemical detection assay for the quantitative determination of monoamines and respective metabolites in six discrete brain regions of mice

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