ParkinsonCanadaV1, PubMed, Checkpoint, bibRecord, 000828

The pharmacology of L-DOPA-induced dyskinesia in Parkinson's disease.

Identifieur interne : 000828 ( PubMed/Checkpoint ); précédent : 000827; suivant : 000829

The pharmacology of L-DOPA-induced dyskinesia in Parkinson's disease.

Auteurs : Philippe Huot [Canada] ; Tom H. Johnston ; James B. Koprich ; Susan H. Fox ; Jonathan M. Brotchie

Source :

Pharmacological reviews [ 1521-0081 ] ; 2013.

RBID : pubmed:23319549

English descriptors

KwdEn :
- Animals, Antiparkinson Agents (adverse effects), Basal Ganglia (physiology), Dopamine Agents (adverse effects), Dyskinesia, Drug-Induced (etiology), Dyskinesia, Drug-Induced (metabolism), Dyskinesia, Drug-Induced (physiopathology), Humans, Levodopa (adverse effects), Parkinson Disease (drug therapy), Parkinson Disease (metabolism), Parkinson Disease (physiopathology), Synaptic Transmission (physiology).
MESH :
- chemical , adverse effects : Antiparkinson Agents, Dopamine Agents, Levodopa.
- drug therapy : Parkinson Disease.
- etiology : Dyskinesia, Drug-Induced.
- metabolism : Dyskinesia, Drug-Induced, Parkinson Disease.
- physiology : Basal Ganglia, Synaptic Transmission.
- physiopathology : Dyskinesia, Drug-Induced, Parkinson Disease.
- Animals, Humans.

Abstract

L-3,4-Dihydroxyphenylalanine (L-DOPA) remains the most effective symptomatic treatment of Parkinson's disease (PD). However, long-term administration of L-DOPA is marred by the emergence of abnormal involuntary movements, i.e., L-DOPA-induced dyskinesia (LID). Years of intensive research have yielded significant progress in the quest to elucidate the mechanisms leading to the development and expression of dyskinesia and maintenance of the dyskinetic state, but the search for a complete understanding is still ongoing. Herein, we summarize the current knowledge of the pharmacology of LID in PD. Specifically, we review evidence gathered from postmortem and pharmacological studies, both preclinical and clinical, and discuss the involvement of dopaminergic and nondopaminergic systems, including glutamatergic, opioid, serotonergic, γ-aminobutyric acid (GABA)-ergic, adenosine, cannabinoid, adrenergic, histaminergic, and cholinergic systems. Moreover, we discuss changes occurring in transcription factors, intracellular signaling, and gene expression in the dyskinetic phenotype. Inasmuch as a multitude of neurotransmitters and receptors play a role in the etiology of dyskinesia, we propose that to optimally alleviate this motor complication, it may be necessary to develop combined treatment approaches that will target simultaneously more than one neurotransmitter system. This could be achieved via three ways as follows: 1) by developing compounds that will interact simultaneously to a multitude of receptors with the required agonist/antagonist effect at each target, 2) by targeting intracellular signaling cascades where the signals mediated by multiple receptors converge, and/or 3) to regulate gene expression in a manner that has effects on signaling by multiple pathways.

DOI: 10.1124/pr.111.005678
PubMed: 23319549

Affiliations:

Canada

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Le document en format XML

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<front><div type="abstract" xml:lang="en">L-3,4-Dihydroxyphenylalanine (L-DOPA) remains the most effective symptomatic treatment of Parkinson's disease (PD). However, long-term administration of L-DOPA is marred by the emergence of abnormal involuntary movements, i.e., L-DOPA-induced dyskinesia (LID). Years of intensive research have yielded significant progress in the quest to elucidate the mechanisms leading to the development and expression of dyskinesia and maintenance of the dyskinetic state, but the search for a complete understanding is still ongoing. Herein, we summarize the current knowledge of the pharmacology of LID in PD. Specifically, we review evidence gathered from postmortem and pharmacological studies, both preclinical and clinical, and discuss the involvement of dopaminergic and nondopaminergic systems, including glutamatergic, opioid, serotonergic, γ-aminobutyric acid (GABA)-ergic, adenosine, cannabinoid, adrenergic, histaminergic, and cholinergic systems. Moreover, we discuss changes occurring in transcription factors, intracellular signaling, and gene expression in the dyskinetic phenotype. Inasmuch as a multitude of neurotransmitters and receptors play a role in the etiology of dyskinesia, we propose that to optimally alleviate this motor complication, it may be necessary to develop combined treatment approaches that will target simultaneously more than one neurotransmitter system. This could be achieved via three ways as follows: 1) by developing compounds that will interact simultaneously to a multitude of receptors with the required agonist/antagonist effect at each target, 2) by targeting intracellular signaling cascades where the signals mediated by multiple receptors converge, and/or 3) to regulate gene expression in a manner that has effects on signaling by multiple pathways.</div>
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	La maladie de Parkinson au Canada (serveur d'exploration)
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La maladie de Parkinson au Canada (serveur d'exploration)

The pharmacology of L-DOPA-induced dyskinesia in Parkinson's disease.

The pharmacology of L-DOPA-induced dyskinesia in Parkinson's disease.

Source :

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

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Pour générer des pages wiki