Interaction between Monoamine Oxidase B Inhibitors and Selective Serotonin Reuptake Inhibitors

Aboukarr, Abdullah; Giudice, Mirella

doi:10.4212/cjhp.v71i3.2586

Cited by 19 publications

(23 citation statements)

References 28 publications

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“…Concerns exist regarding the safety of combining MAOBIs with antidepressants, because of the risk of the potentially fatal serotonin syndrome, although serotonin syndrome is rarely induced by MAOBIs such as selegiline and rasagiline [ 16 , 17 , 18 , 19 , 20 ]. However, there are no studies assessing serotonin syndrome in patients concomitantly treated with safinamide and antidepressants.…”

Section: Introductionmentioning

confidence: 99%

Impact of SAfinamide on Depressive Symptoms in Parkinson’s Disease Patients (SADness-PD Study): A Multicenter Retrospective Study

et al. 2021

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Background: We aimed to assess the effects of safinamide on depression, motor symptoms, and the serotonin syndrome related to its co-administration with antidepressants in patients with Parkinson’s disease (PD). Methods: We retrospectively analyzed the data of patients at 1 and 3 months of follow-up compared to baseline. Results: n = 82 (safinamide 50 mg = 22, 100 mg = 60, with antidepressants = 44). First, we found improvement in depression (Hamilton Depression Rating Scale: −6 ± 5.10 at 1 month and −7.27 ± 5.10 at 3 months, p < 0.0001; Patient Global Impression of Improvement Scale: 60.3% and 69.5% of patients at 1 and 3 months reported some improvement). Second, safinamide improved the daily life activities and motor symptoms/motor complications (Unified Parkinson’s Disease Rating Scale (UPDRS-II): −2.51 ± 6.30 and −2.47 ± 6.11 at 1 and 3 months, p < 0.0001; III: −3.58 ± 8.68 and −4.03 ± 8.95 at 1 and 3 months, p < 0.0001; IV: −0.61 ± 2.61 and −0.8 ± 2.53 at 1 and 3 months, p < 0.0001). Third, 7.31% and 8.53% of patients developed non-severe adverse events related to safinamide at 1 and 3 months. Serotonin syndrome was not observed in the patients treated with antidepressants; some isolated serotonin syndrome symptoms were reported. Conclusions: Safinamide could be useful for treating depression in PD; it was effective for motor symptoms and motor complications and safe even when co-administered with antidepressants.

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Section: Introductionmentioning

confidence: 99%

Impact of SAfinamide on Depressive Symptoms in Parkinson’s Disease Patients (SADness-PD Study): A Multicenter Retrospective Study

et al. 2021

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“…A recent literature review was conducted to investigate the potential interaction between MAO-B inhibitors and SSRIs in patients with PD [41]. Based on the literature evidence [42,43], the authors concluded that SSRIs and MAO-B inhibitors could be administered concomitantly if they do not exceed the recommended doses and the SSRI is administered at the lower end of the therapeutic range [41].…”

Section: Concomitant Use Of Safinamide and Antidepressantsmentioning

confidence: 99%

“…Conclusion: Although there is a rational basis on the negative interaction between safinamide and antidepressants, there is not enough evidence supporting this effect to date [24,41,44]. Level of agreement: 100%.…”

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confidence: 96%

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A Spanish Consensus on the Use of Safinamide for Parkinson’s Disease in Clinical Practice

et al. 2020

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Safinamide is an approved drug for the treatment of motor fluctuations in Parkinson’s disease (PD). Scarce data are available on its use in clinical practice. A group of Spanish movement disorders specialists was convened to review the use of safinamide across different clinical scenarios that may guide neurologists in clinical practice. Eight specialists with recognized expertise in PD management elaborated the statements based on available evidence in the literature and on their clinical experience. The RAND/UCLA method was carried, with final conclusions accepted after a 2-round modified Delphi process. Higher level of agreement between panellists was reached for the following statements. Safinamide significantly improves mean daily OFF time without troublesome dyskinesias. Adjunctive treatment with safinamide is associated with motor improvements in patients with mid-to-late PD. The efficacy of safinamide on motor fluctuations is maintained at long-term, with no increase over time in dyskinesias severity. The clinical benefits of safinamide on pain and depression remain unclear. Safinamide presents a similar incidence of adverse events compared with placebo. The efficacy and safety of safinamide shown in the pivotal clinical trials are reproduced in clinical practice, with improvement of parkinsonian symptoms, decrease of daily OFF time, control of dyskinesias at the long term, and good tolerability and safety.

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“…Cognitive decline in Alzheimer’s disease (AD) is associated with the interplay among different neurotransmitters, including dopamine, serotonin, noradrenaline, or glutamate (Martorana et al ). Among the symptoms in PD, AD, and Huntington’s Disease (HD), depression is commonly found accompanying these diseases (Grimes et al ; Beglinger et al ; Cooney and Stacy ; Aboukarr and Giudice ), making the treatment more complex.…”

mentioning

confidence: 99%

Drug testing complementary metal‐oxide‐semiconductor chip reveals drug modulation of transmitter release for potential therapeutic applications

Huang

Rathore

Lindau

2019

Journal of Neurochemistry

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Neurodegenerative diseases, such as Parkinson’s disease, Alzheimer’s disease, and Huntington’s disease, are considered incurable and significantly reduce the quality of life of the patients. A variety of drugs that modulate neurotransmitter levels have been used for the treatment of the neurodegenerative diseases but with limited efficacy. In this work, an amperometric complementary metal‐oxide‐semiconductor (CMOS) chip is used for high‐throughput drug testing with respect to the modulation of transmitter release from single vesicles using chromaffin cells prepared from bovine adrenal glands as a model system. Single chromaffin cell amperometry was performed with high efficiency on the surface‐modified CMOS chip and follow‐up whole‐cell patch‐clamp experiments were performed to determine the readily releasable pool sizes. We show that the antidepressant drug bupropion significantly increases the amount of neurotransmitter released in individual quantal release events. The antidepressant drug citalopram accelerates rapid neurotransmitter release following stimulation and follow‐up patch‐clamp experiments reveal that this is because of the increase in the pool of readily releasable vesicles. These results shed light on the mechanisms by which bupropion and citalopram may be potentially effective in the treatment of neurodegenerative diseases. These results demonstrate that the CMOS amperometry chip technology is an excellent tool for drug testing to determine the specific mechanisms by which they modulate neurotransmitter release.

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Interaction between Monoamine Oxidase B Inhibitors and Selective Serotonin Reuptake Inhibitors

Cited by 19 publications

References 28 publications

Impact of SAfinamide on Depressive Symptoms in Parkinson’s Disease Patients (SADness-PD Study): A Multicenter Retrospective Study

Impact of SAfinamide on Depressive Symptoms in Parkinson’s Disease Patients (SADness-PD Study): A Multicenter Retrospective Study

A Spanish Consensus on the Use of Safinamide for Parkinson’s Disease in Clinical Practice

Drug testing complementary metal‐oxide‐semiconductor chip reveals drug modulation of transmitter release for potential therapeutic applications

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