Challenging the Serotonergic System in Parkinson Disease Patients

Scholtissen, Bart; Verhey, Frans R.J.; Adam, Jos J.; Weber, Wim M.; Leentjens, Albert F.G.

doi:10.1097/01.wnf.0000229013.95927.c7

Cited by 23 publications

(11 citation statements)

References 34 publications

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“…This effect may participate in the emergence of cognitive and depressive disorders after short-and long-term treatment in PD (Zesiewicz and Hauser, 2002;Scholtissen et al, 2006). Finally, we provide evidence that the combined approaches, while not aggravating the decrease in 5-HT release, could limit side effects associated with excessive DA transmission in the brain.…”

Section: Stn-hfs and L-dopa In The Treatment Of Pdmentioning

confidence: 82%

“…While the two different approaches are very efficient in improving the motor symptoms of the disease, their motor benefits are burdened by the occurrence of psychiatric side effects, including cognitive impairments and mood disorders (Piasecki and Jefferson, 2004;Haber and Brucker, 2009;Van Rooden et al, 2009). Compelling evidence indicates that the serotonergic system, considered as an etiologic and pathophysiological factor in PD (Zesiewicz and Hauser, 2002;Scholtissen et al, 2006), plays a role in cognitive and mood disorders (Piñeyro and Blier, 1999;Bhagwagar et al, 2002). Changes in serotonergic function could participate in nonmotor side effects induced by antiparkinsonian therapies (Melamed et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

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High-Frequency Stimulation of the Subthalamic Nucleus and l-3,4-Dihydroxyphenylalanine InhibitIn VivoSerotonin Release in the Prefrontal Cortex and Hippocampus in a Rat Model of Parkinson's Disease

Navailles¹,

Benazzouz²,

Bioulac³

et al. 2010

J. Neurosci.

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Section: Stn-hfs and L-dopa In The Treatment Of Pdmentioning

confidence: 82%

Section: Introductionmentioning

confidence: 99%

High-Frequency Stimulation of the Subthalamic Nucleus and l-3,4-Dihydroxyphenylalanine InhibitIn VivoSerotonin Release in the Prefrontal Cortex and Hippocampus in a Rat Model of Parkinson's Disease

Navailles¹,

Benazzouz²,

Bioulac³

et al. 2010

J. Neurosci.

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“…was administered. Citalopram had a negative effect on visual verbal learning task, exacerbated subscores of depression, anger, and anxiety, and had no effect on concept shifting task, UPDRS part III, or reaction time [152]. …”

Section: Sert 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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“…Second, in addition to the main dopaminergic dysfunction, other neurotransmitters are dysfunctional with different degrees in PD, including acetylcholine, serotonin and norepinephrine [Baloyannis et al 2006;Bohnen et al 2006;Guttman et al 2007], although their role in cognitive dysfunction is partially unknown [Calabresi et al 2006;Marsh et al 2009;Scholtissen et al 2006] and deserves further empirical investigation.…”

Section: Future Directionsmentioning

confidence: 99%

Acute and chronic cognitive effects of levodopa and dopamine agonists on patients with Parkinson’s disease: a review

Poletti

Bonuccelli

2012

Therapeutic Advances in Psychopharmacology

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Abstract:The spatiotemporal progression of dopamine depletion in Parkinson's disease (PD) provides a special model for assessing dopaminergic effects on neural systems with differential baseline dopamine levels. This study aims at reviewing cognitive effects of dopaminergic stimulation in PD. While considering dopaminergic drugs (levodopa or dopamine agonists), temporal intervals (acute or chronic) and cognitive domains, we found that empirical evidence was almost focused on acute effects of levodopa on executive functions. The paucity of empirical evidence suggests that no meaningful conclusions can be actually drawn and further research is needed in relation to: (1) other cognitive domains; (2) the acute cognitive effects of dopamine agonists, as compared with levodopa; (3) possible differences between cognitive effects of different dopamine agonists; (4) the cognitive effects of chronic dopaminergic therapies. The latter issue is of particular clinical interest considering that many PD patients present a mild cognitive impairment: is this cognitive feature worsened or improved by the prolonged dopaminergic therapy? In addition to the potential risk of inducing dyskinesia and behavioral side effects such as impulse control disorders, also cognitive effects of prolonged dopaminergic treatments should be taken in account by clinicians in order to anticipate or to delay their prescription to PD patients.

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Challenging the Serotonergic System in Parkinson Disease Patients

Cited by 23 publications

References 34 publications

High-Frequency Stimulation of the Subthalamic Nucleus and l-3,4-Dihydroxyphenylalanine InhibitIn VivoSerotonin Release in the Prefrontal Cortex and Hippocampus in a Rat Model of Parkinson's Disease

High-Frequency Stimulation of the Subthalamic Nucleus and l-3,4-Dihydroxyphenylalanine InhibitIn VivoSerotonin Release in the Prefrontal Cortex and Hippocampus in a Rat Model of Parkinson's Disease

Monoamine Reuptake Inhibitors in Parkinson’s Disease

Acute and chronic cognitive effects of levodopa and dopamine agonists on patients with Parkinson’s disease: a review

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