Novel nondopaminergic targets for motor features of Parkinson's disease: review of recent trials.
Identifieur interne : 000876 ( Main/Exploration ); précédent : 000875; suivant : 000877Novel nondopaminergic targets for motor features of Parkinson's disease: review of recent trials.
Auteurs : Lorraine V. Kalia [Canada] ; Jonathan M. Brotchie ; Susan H. FoxSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2013.
English descriptors
- KwdEn :
- Acetylcholine (physiology), Adenosine A3 Receptor Antagonists (therapeutic use), Adrenergic Uptake Inhibitors (therapeutic use), Animals, Antiparkinson Agents (pharmacology), Antiparkinson Agents (therapeutic use), Caffeine (therapeutic use), Cholinesterase Inhibitors (therapeutic use), GABA Modulators (therapeutic use), Genetic Therapy, Glutamate Decarboxylase (genetics), Histamine H2 Antagonists (therapeutic use), Humans, Movement Disorders (drug therapy), Movement Disorders (etiology), Movement Disorders (physiopathology), Nicotinic Agonists (therapeutic use), Parkinson Disease (complications), Parkinson Disease (drug therapy), Parkinson Disease (physiopathology), Phosphodiesterase Inhibitors (therapeutic use), Receptor, Adenosine A2A (drug effects), Receptors, N-Methyl-D-Aspartate (antagonists & inhibitors), Serotonin Receptor Agonists (therapeutic use).
- MESH :
- chemical , antagonists & inhibitors : Receptors, N-Methyl-D-Aspartate.
- chemical , drug effects : Receptor, Adenosine A2A.
- chemical , genetics : Glutamate Decarboxylase.
- chemical , pharmacology : Antiparkinson Agents.
- chemical , physiology : Acetylcholine.
- chemical , therapeutic use : Adenosine A3 Receptor Antagonists, Adrenergic Uptake Inhibitors, Antiparkinson Agents, Caffeine, Cholinesterase Inhibitors, GABA Modulators, Histamine H2 Antagonists, Nicotinic Agonists, Phosphodiesterase Inhibitors, Serotonin Receptor Agonists.
- complications : Parkinson Disease.
- drug therapy : Movement Disorders, Parkinson Disease.
- etiology : Movement Disorders.
- physiopathology : Movement Disorders, Parkinson Disease.
- Animals, Genetic Therapy, Humans.
Abstract
Neurotransmitters other than dopamine are recognized as having modulatory roles within the basal ganglia and can influence the basal ganglia dopaminergic system to alter activity of the direct and indirect pathways. Many nondopaminergic neurotransmitter systems have been implicated in the mechanisms contributing to the motor features of Parkinson's disease (PD). Thus, it is now well established that neurotransmitter systems, including glutamatergic, GABAergic, cholinergic, noradrenergic, serotonergic, opioidergic, histaminergic, and adenosinergic systems, are affected in the pathogenesis of PD. Nondopaminergic neurotransmitter systems are thus targets for the development of novel therapies for motor symptoms and motor complications in PD. Over the last 5 years, more than 20 randomized, control trials (RCTs) in PD investigating drugs that target several of these nondopaminergic neurotransmitter systems for the treatment of motor features have been completed. There are at least 15 additional RCTs that are ongoing or planned. Here, we review these RCTs to highlight the potential nondopaminergic pharmacological therapies for treatment of motor features of PD. Nondopaminergic drugs are not expected to replace dopaminergic strategies, but further development of these drugs will likely yield novel approaches with positive clinical implications.
DOI: 10.1002/mds.25273
PubMed: 23225267
Affiliations:
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Le document en format XML
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Brotchie</name></author><author><name sortKey="Fox, Susan H" sort="Fox, Susan H" uniqKey="Fox S" first="Susan H" last="Fox">Susan H. 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Fox</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acetylcholine (physiology)</term><term>Adenosine A3 Receptor Antagonists (therapeutic use)</term><term>Adrenergic Uptake Inhibitors (therapeutic use)</term><term>Animals</term><term>Antiparkinson Agents (pharmacology)</term><term>Antiparkinson Agents (therapeutic use)</term><term>Caffeine (therapeutic use)</term><term>Cholinesterase Inhibitors (therapeutic use)</term><term>GABA Modulators (therapeutic use)</term><term>Genetic Therapy</term><term>Glutamate Decarboxylase (genetics)</term><term>Histamine H2 Antagonists (therapeutic use)</term><term>Humans</term><term>Movement Disorders (drug therapy)</term><term>Movement Disorders (etiology)</term><term>Movement Disorders (physiopathology)</term><term>Nicotinic Agonists (therapeutic use)</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (physiopathology)</term><term>Phosphodiesterase Inhibitors (therapeutic use)</term><term>Receptor, Adenosine A2A (drug effects)</term><term>Receptors, N-Methyl-D-Aspartate (antagonists & inhibitors)</term><term>Serotonin Receptor Agonists (therapeutic use)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Receptors, N-Methyl-D-Aspartate</term></keywords><keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Receptor, Adenosine A2A</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Glutamate Decarboxylase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antiparkinson Agents</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Acetylcholine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Adenosine A3 Receptor Antagonists</term><term>Adrenergic Uptake Inhibitors</term><term>Antiparkinson Agents</term><term>Caffeine</term><term>Cholinesterase Inhibitors</term><term>GABA Modulators</term><term>Histamine H2 Antagonists</term><term>Nicotinic Agonists</term><term>Phosphodiesterase Inhibitors</term><term>Serotonin Receptor Agonists</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Movement Disorders</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Movement Disorders</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Movement Disorders</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Genetic Therapy</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Neurotransmitters other than dopamine are recognized as having modulatory roles within the basal ganglia and can influence the basal ganglia dopaminergic system to alter activity of the direct and indirect pathways. Many nondopaminergic neurotransmitter systems have been implicated in the mechanisms contributing to the motor features of Parkinson's disease (PD). Thus, it is now well established that neurotransmitter systems, including glutamatergic, GABAergic, cholinergic, noradrenergic, serotonergic, opioidergic, histaminergic, and adenosinergic systems, are affected in the pathogenesis of PD. Nondopaminergic neurotransmitter systems are thus targets for the development of novel therapies for motor symptoms and motor complications in PD. Over the last 5 years, more than 20 randomized, control trials (RCTs) in PD investigating drugs that target several of these nondopaminergic neurotransmitter systems for the treatment of motor features have been completed. There are at least 15 additional RCTs that are ongoing or planned. Here, we review these RCTs to highlight the potential nondopaminergic pharmacological therapies for treatment of motor features of PD. Nondopaminergic drugs are not expected to replace dopaminergic strategies, but further development of these drugs will likely yield novel approaches with positive clinical implications.</div></front></TEI><affiliations><list><country><li>Canada</li></country></list><tree><noCountry><name sortKey="Brotchie, Jonathan M" sort="Brotchie, Jonathan M" uniqKey="Brotchie J" first="Jonathan M" last="Brotchie">Jonathan M. Brotchie</name><name sortKey="Fox, Susan H" sort="Fox, Susan H" uniqKey="Fox S" first="Susan H" last="Fox">Susan H. Fox</name></noCountry><country name="Canada"><noRegion><name sortKey="Kalia, Lorraine V" sort="Kalia, Lorraine V" uniqKey="Kalia L" first="Lorraine V" last="Kalia">Lorraine V. Kalia</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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