Bupropion abates dopamine agonist-mediated compulsive behaviors in Parkinson's disease

Benincasa, Dario; Pellicano, Clelia; Fanciulli, Alessandra; Pontieri, Francesco E.

doi:10.1002/mds.23395

Cited by 9 publications

(13 citation statements)

References 6 publications

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“…id) significantly alleviated dopamine agonist-induced compulsive behaviour and depressive symptoms. Bupropion had no effect on Parkinsonism and did not trigger or exacerbate dyskinesia [594]. …”

Section: Dat = Net Inhibitorsmentioning

confidence: 99%

Monoamine Reuptake Inhibitors in Parkinson’s Disease

Huot

Fox

Brotchie

2015

Parkinson's Disease

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The motor manifestations of Parkinson's disease (PD) are secondary to a dopamine deficiency in the striatum. However, the degenerative process in PD is not limited to the dopaminergic system and also affects serotonergic and noradrenergic neurons. Because they can increase monoamine levels throughout the brain, monoamine reuptake inhibitors (MAUIs) represent potential therapeutic agents in PD. However, they are seldom used in clinical practice other than as antidepressants and wake-promoting agents. This review article summarises all of the available literature on use of 50 MAUIs in PD. The compounds are divided according to their relative potency for each of the monoamine transporters. Despite wide discrepancy in the methodology of the studies reviewed, the following conclusions can be drawn: (1) selective serotonin transporter (SERT), selective noradrenaline transporter (NET), and dual SERT/NET inhibitors are effective against PD depression; (2) selective dopamine transporter (DAT) and dual DAT/NET inhibitors exert an anti-Parkinsonian effect when administered as monotherapy but do not enhance the anti-Parkinsonian actions of L-3,4-dihydroxyphenylalanine (L-DOPA); (3) dual DAT/SERT inhibitors might enhance the anti-Parkinsonian actions of L-DOPA without worsening dyskinesia; (4) triple DAT/NET/SERT inhibitors might exert an anti-Parkinsonian action as monotherapy and might enhance the anti-Parkinsonian effects of L-DOPA, though at the expense of worsening dyskinesia.

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Section: Dat = Net Inhibitorsmentioning

confidence: 99%

Monoamine Reuptake Inhibitors in Parkinson’s Disease

Huot

Fox

Brotchie

2015

Parkinson's Disease

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“…[54][55][56] To date, it was repeatedly recommended as treatment of choice for depression in PD patients. [57][58][59] Monotherapy with nomifensine showed positive effects in l-dopa naïve PD patients. Combination of nomifensine with l-dopa provided controversial outcomes.…”

Section: Clinical Trialsmentioning

confidence: 95%

Experimental Dopamine Reuptake Inhibitors in Parkinson’s Disease: A Review of the Evidence

Müller¹

2021

JEP

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Parkinson's disease (PD) is the second most chronic neurodegenerative disorder worldwide. Deficit of monoamines, particularly dopamine, causes an individually varying compilation of motor and non-motor features. Constraint of presynaptic uptake extends monoamine stay in the synaptic cleft. This review discusses possible benefits of dopamine reuptake inhibition for the treatment of PD. Translation of this pharmacologic principle into positive clinical study results failed to date. Past clinical trial designs did not consider a mandatory, concomitant stable inhibition of glial monoamine turnover, i.e. with monoamine oxidase B inhibitors. These studies focused on improvement of motor behavior and levodopa associated motor complications, which are fluctuations of motor and non-motor behavior. Future clinical investigations in early, levodopa-and dopamine agonist naïve patients shall also aim on alleviation of non-motor symptoms, like fatigue, apathy or cognitive slowing. Oral levodopa/dopa decarboxylase inhibitor application is inevitably necessary with advance of PD. Monoamine reuptake (MRT) inhibition improves the efficacy of levodopa, the blood brain barrier crossing metabolic precursor of dopamine. The pulsatile brain delivery pattern of orally administered levodopa containing formulations results in synaptic dopamine variability. Ups and downs of dopamine counteract the physiologic principle of continuous neurotransmission, particularly in nigrostriatal, respectively mesocorticolimbic pathways, both of which regulate motor respectively non-motor behavior. Thus synaptic dopamine pulsatility overwhelms the existing buffering capacity. Onset of motor and non-motor complications occurs. Future MRT inhibitor studies shall focus on a stabilizing and preventive effect on levodopa related fluctuations of motor and non-motor behavior. Their long-term study designs in advanced levodopa treated patients shall allow a cautious adaptation of oral l-dopa therapy combined with a mandatory inhibition of glial monoamine turnover. Then the evidence for a preventive and beneficial, symptomatic effect of MRT inhibition on motor and non-motor complications will become more likely.

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“… Co-administration of Memantine might be responsible for PSM. Benincasa, 2011 [ 30 ] Europe (Spain) Case report 3 females (mean age 53.7 years) with PD who developed compulsive eating after dopaminergic medications (ropinirole and pramipexole) with comorbid depressive symptoms (HAMD mean score: 14.7). Compulsive behavior + depressive symptoms 150 mg/day.…”

Section: Methodsmentioning

confidence: 99%

Clinical uses of Bupropion in patients with Parkinson’s disease and comorbid depressive or neuropsychiatric symptoms: a scoping review

et al. 2022

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Objective Bupropion, an antidepressant inhibiting the reuptake of dopamine and noradrenaline, should be useful to treat depressive symptoms in patients with Parkinson’s disease (PD). Limited and conflicting literature data questioned its effectiveness and safety in depressed PD patients and extended its use to other neuropsychiatric symptoms associated with this disorder. Design The databases PubMed, Embase, Web of Sciences, Cochrane Library, and the grey literature were searched. Following a scoping review methodology, articles focusing on Bupropion uses in PD patients who manifested depressive or other neuropsychiatric alterations were reviewed. Results Twenty-three articles were selected, including 7 original articles, 3 systematic reviews or meta-analyses, 11 case reports, 1 clinical guideline, and 1 expert opinion. Bupropion showed considerable effectiveness in reducing depressive symptoms, particularly in relation to apathy. Solitary findings showed a restorative effect on compulsive behaviour secondary to treatment with dopamine as well as on anxiety symptoms. The effect on motor symptoms remains controversial. The safety profile of this medication seems positive, but additional precautions should be used in subjects with psychotic symptoms. Conclusion The available literature lacks good evidence to support the use of Bupropion in PD patients presenting depressive symptoms. Further investigations are needed to extend and confirm reported findings and to produce accurate clinical guidelines.

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Bupropion abates dopamine agonist-mediated compulsive behaviors in Parkinson's disease

Cited by 9 publications

References 6 publications

Monoamine Reuptake Inhibitors in Parkinson’s Disease

Monoamine Reuptake Inhibitors in Parkinson’s Disease

Experimental Dopamine Reuptake Inhibitors in Parkinson’s Disease: A Review of the Evidence

Clinical uses of Bupropion in patients with Parkinson’s disease and comorbid depressive or neuropsychiatric symptoms: a scoping review

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