Priorities in Parkinson's disease research.
Identifieur interne : 000D11 ( Ncbi/Curation ); précédent : 000D10; suivant : 000D12Priorities in Parkinson's disease research.
Auteurs : Wassilios G. Meissner [France] ; Mark Frasier ; Thomas Gasser ; Christopher G. Goetz ; Andres Lozano ; Paola Piccini ; José A. Obeso ; Olivier Rascol ; Anthony Schapira ; Valerie Voon ; David M. Weiner ; François Tison ; Erwan BezardSource :
- Nature reviews. Drug discovery [ 1474-1784 ] ; 2011.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Dopamine.
- chemical , pharmacology : Antiparkinson Agents.
- drug therapy : Parkinson Disease.
- methods : Clinical Trials as Topic.
- pathology : Neurons.
- physiopathology : Parkinson Disease.
- Animals, Disease Models, Animal, Drug Delivery Systems, Drug Design, Drug Evaluation, Preclinical, Humans.
Abstract
The loss of dopaminergic neurons in the substantia nigra pars compacta leads to the characteristic motor symptoms of Parkinson's disease: bradykinesia, rigidity and resting tremors. Although these symptoms can be improved using currently available dopamine replacement strategies, there is still a need to improve current strategies of treating these symptoms, together with a need to alleviate non-motor symptoms of the disease. Moreover, treatments that provide neuroprotection and/or disease-modifying effects remain an urgent unmet clinical need. This Review describes the most promising biological targets and therapeutic agents that are currently being assessed to address these treatment goals. Progress will rely on understanding genetic mutations or susceptibility factors that lead to Parkinson's disease, better translation between preclinical animal models and clinical research, and improving the design of future clinical trials.
DOI: 10.1038/nrd3430
PubMed: 21532567
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Goetz</name></author><author><name sortKey="Lozano, Andres" sort="Lozano, Andres" uniqKey="Lozano A" first="Andres" last="Lozano">Andres Lozano</name></author><author><name sortKey="Piccini, Paola" sort="Piccini, Paola" uniqKey="Piccini P" first="Paola" last="Piccini">Paola Piccini</name></author><author><name sortKey="Obeso, Jose A" sort="Obeso, Jose A" uniqKey="Obeso J" first="José A" last="Obeso">José A. Obeso</name></author><author><name sortKey="Rascol, Olivier" sort="Rascol, Olivier" uniqKey="Rascol O" first="Olivier" last="Rascol">Olivier Rascol</name></author><author><name sortKey="Schapira, Anthony" sort="Schapira, Anthony" uniqKey="Schapira A" first="Anthony" last="Schapira">Anthony Schapira</name></author><author><name sortKey="Voon, Valerie" sort="Voon, Valerie" uniqKey="Voon V" first="Valerie" last="Voon">Valerie Voon</name></author><author><name sortKey="Weiner, David M" sort="Weiner, David M" uniqKey="Weiner D" first="David M" last="Weiner">David M. 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Meissner</name><affiliation wicri:level="1"><nlm:affiliation>Service de Neurologie et Centre de référence atrophie multisystématisée, CHU de Bordeaux, Avenue Magellan F-33604 Pessac France. wassilios.meissner@chu-bordeaux.fr</nlm:affiliation><country wicri:rule="url">France</country></affiliation></author><author><name sortKey="Frasier, Mark" sort="Frasier, Mark" uniqKey="Frasier M" first="Mark" last="Frasier">Mark Frasier</name></author><author><name sortKey="Gasser, Thomas" sort="Gasser, Thomas" uniqKey="Gasser T" first="Thomas" last="Gasser">Thomas Gasser</name></author><author><name sortKey="Goetz, Christopher G" sort="Goetz, Christopher G" uniqKey="Goetz C" first="Christopher G" last="Goetz">Christopher G. Goetz</name></author><author><name sortKey="Lozano, Andres" sort="Lozano, Andres" uniqKey="Lozano A" first="Andres" last="Lozano">Andres Lozano</name></author><author><name sortKey="Piccini, Paola" sort="Piccini, Paola" uniqKey="Piccini P" first="Paola" last="Piccini">Paola Piccini</name></author><author><name sortKey="Obeso, Jose A" sort="Obeso, Jose A" uniqKey="Obeso J" first="José A" last="Obeso">José A. Obeso</name></author><author><name sortKey="Rascol, Olivier" sort="Rascol, Olivier" uniqKey="Rascol O" first="Olivier" last="Rascol">Olivier Rascol</name></author><author><name sortKey="Schapira, Anthony" sort="Schapira, Anthony" uniqKey="Schapira A" first="Anthony" last="Schapira">Anthony Schapira</name></author><author><name sortKey="Voon, Valerie" sort="Voon, Valerie" uniqKey="Voon V" first="Valerie" last="Voon">Valerie Voon</name></author><author><name sortKey="Weiner, David M" sort="Weiner, David M" uniqKey="Weiner D" first="David M" last="Weiner">David M. Weiner</name></author><author><name sortKey="Tison, Francois" sort="Tison, Francois" uniqKey="Tison F" first="François" last="Tison">François Tison</name></author><author><name sortKey="Bezard, Erwan" sort="Bezard, Erwan" uniqKey="Bezard E" first="Erwan" last="Bezard">Erwan Bezard</name></author></analytic><series><title level="j">Nature reviews. Drug discovery</title><idno type="eISSN">1474-1784</idno><imprint><date when="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antiparkinson Agents (pharmacology)</term><term>Clinical Trials as Topic (methods)</term><term>Disease Models, Animal</term><term>Dopamine (metabolism)</term><term>Drug Delivery Systems</term><term>Drug Design</term><term>Drug Evaluation, Preclinical</term><term>Humans</term><term>Neurons (pathology)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (physiopathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antiparkinson Agents</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Clinical Trials as Topic</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Drug Delivery Systems</term><term>Drug Design</term><term>Drug Evaluation, Preclinical</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The loss of dopaminergic neurons in the substantia nigra pars compacta leads to the characteristic motor symptoms of Parkinson's disease: bradykinesia, rigidity and resting tremors. Although these symptoms can be improved using currently available dopamine replacement strategies, there is still a need to improve current strategies of treating these symptoms, together with a need to alleviate non-motor symptoms of the disease. Moreover, treatments that provide neuroprotection and/or disease-modifying effects remain an urgent unmet clinical need. This Review describes the most promising biological targets and therapeutic agents that are currently being assessed to address these treatment goals. Progress will rely on understanding genetic mutations or susceptibility factors that lead to Parkinson's disease, better translation between preclinical animal models and clinical research, and improving the design of future clinical trials.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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