Are dopamine receptor agonists neuroprotective in Parkinson's disease?
Identifieur interne : 000249 ( PubMed/Corpus ); précédent : 000248; suivant : 000250Are dopamine receptor agonists neuroprotective in Parkinson's disease?
Auteurs : W Le ; J. JankovicSource :
- Drugs & aging [ 1170-229X ] ; 2001.
English descriptors
- KwdEn :
- Animals, Antiparkinson Agents (pharmacology), Antiparkinson Agents (therapeutic use), Apomorphine (pharmacology), Benzothiazoles, Bromocriptine (pharmacology), Cell Culture Techniques, Clinical Trials as Topic, Dopamine Agonists (pharmacology), Dopamine Agonists (therapeutic use), Humans, Indoles (pharmacology), Models, Animal, Neuroprotective Agents (pharmacology), Neuroprotective Agents (therapeutic use), Parkinson Disease (drug therapy), Pergolide (pharmacology), Substantia Nigra (injuries), Thiazoles (pharmacology).
- MESH :
- chemical , pharmacology : Antiparkinson Agents, Apomorphine, Bromocriptine, Dopamine Agonists, Indoles, Neuroprotective Agents, Pergolide, Thiazoles.
- chemical , therapeutic use : Antiparkinson Agents, Dopamine Agonists, Neuroprotective Agents.
- drug therapy : Parkinson Disease.
- injuries : Substantia Nigra.
- Animals, Benzothiazoles, Cell Culture Techniques, Clinical Trials as Topic, Humans, Models, Animal.
Abstract
Dopamine receptor agonists are playing an increasingly important role in the treatment of not only patients with advanced Parkinson's disease and those with levodopa-induced motor fluctuations, but also in the early treatment of the disease. This shift has been largely due to the demonstrated levodopa-sparing effect of dopamine agonists and their putative neuroprotective effect, with evidence for the latter being based largely on experimental in vitro and in vivo studies. In this article we review the evidence for neuroprotection by the dopamine agonists pramipexole, ropinirole, pergolide, bromocriptine and apomorphine in cell cultures and animal models of injury to the substantia nigra. Most of the studies suggest that dopamine agonists may have neuroprotective effects via direct scavenging of free radicals or increasing the activities of radical-scavenging enzymes, and enhancing neurotrophic activity. However, the finding that pramipexole can normalise mitochondrial membrane potential and inhibit activity of caspase-3 in cytoplasmic hybrid cells derived from mitochondrial DNA of patients with nonfamilial Alzheimer's disease suggests an even broader implication for the neuroprotective role of dopamine agonists. Although the clinical evidence for neuroprotection by dopamine agonists is still limited, the preliminary results from several ongoing clinical trials are promising. Several longitudinal studies are currently in progress designed to demonstrate a delay or slowing of progression of Parkinson's disease using various surrogate markers of neuronal degeneration such as 18F-levodopa positron emission tomography and 123I beta-CIT (carbomethoxy-beta-4-iodophenyl-nortropane) single positron emission computed tomography. The results of these experimental and clinical studies will improve our understanding of the action of dopamine agonists and provide critical information needed for planning future therapeutic strategies for Parkinson's disease and related neurodegenerative disorders.
PubMed: 11419913
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pubmed:11419913Le document en format XML
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Jankovic</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2001">2001</date><idno type="RBID">pubmed:11419913</idno><idno type="pmid">11419913</idno><idno type="wicri:Area/PubMed/Corpus">000249</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Are dopamine receptor agonists neuroprotective in Parkinson's disease?</title><author><name sortKey="Le, W D" sort="Le, W D" uniqKey="Le W" first="W" last="Le">W Le</name><affiliation><nlm:affiliation>Department of Neurology, Baylor College of Medicine, Houston, Texas 77030, USA. Weidong@bcm.tmc.edu</nlm:affiliation></affiliation></author><author><name sortKey="Jankovic, J" sort="Jankovic, J" uniqKey="Jankovic J" first="J" last="Jankovic">J. 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This shift has been largely due to the demonstrated levodopa-sparing effect of dopamine agonists and their putative neuroprotective effect, with evidence for the latter being based largely on experimental in vitro and in vivo studies. In this article we review the evidence for neuroprotection by the dopamine agonists pramipexole, ropinirole, pergolide, bromocriptine and apomorphine in cell cultures and animal models of injury to the substantia nigra. Most of the studies suggest that dopamine agonists may have neuroprotective effects via direct scavenging of free radicals or increasing the activities of radical-scavenging enzymes, and enhancing neurotrophic activity. However, the finding that pramipexole can normalise mitochondrial membrane potential and inhibit activity of caspase-3 in cytoplasmic hybrid cells derived from mitochondrial DNA of patients with nonfamilial Alzheimer's disease suggests an even broader implication for the neuroprotective role of dopamine agonists. Although the clinical evidence for neuroprotection by dopamine agonists is still limited, the preliminary results from several ongoing clinical trials are promising. Several longitudinal studies are currently in progress designed to demonstrate a delay or slowing of progression of Parkinson's disease using various surrogate markers of neuronal degeneration such as 18F-levodopa positron emission tomography and 123I beta-CIT (carbomethoxy-beta-4-iodophenyl-nortropane) single positron emission computed tomography. The results of these experimental and clinical studies will improve our understanding of the action of dopamine agonists and provide critical information needed for planning future therapeutic strategies for Parkinson's disease and related neurodegenerative disorders.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">11419913</PMID><DateCreated><Year>2001</Year><Month>06</Month><Day>22</Day></DateCreated><DateCompleted><Year>2001</Year><Month>10</Month><Day>25</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1170-229X</ISSN><JournalIssue CitedMedium="Print"><Volume>18</Volume><Issue>6</Issue><PubDate><Year>2001</Year></PubDate></JournalIssue><Title>Drugs & aging</Title><ISOAbbreviation>Drugs Aging</ISOAbbreviation></Journal><ArticleTitle>Are dopamine receptor agonists neuroprotective in Parkinson's disease?</ArticleTitle><Pagination><MedlinePgn>389-96</MedlinePgn></Pagination><Abstract><AbstractText>Dopamine receptor agonists are playing an increasingly important role in the treatment of not only patients with advanced Parkinson's disease and those with levodopa-induced motor fluctuations, but also in the early treatment of the disease. This shift has been largely due to the demonstrated levodopa-sparing effect of dopamine agonists and their putative neuroprotective effect, with evidence for the latter being based largely on experimental in vitro and in vivo studies. In this article we review the evidence for neuroprotection by the dopamine agonists pramipexole, ropinirole, pergolide, bromocriptine and apomorphine in cell cultures and animal models of injury to the substantia nigra. Most of the studies suggest that dopamine agonists may have neuroprotective effects via direct scavenging of free radicals or increasing the activities of radical-scavenging enzymes, and enhancing neurotrophic activity. However, the finding that pramipexole can normalise mitochondrial membrane potential and inhibit activity of caspase-3 in cytoplasmic hybrid cells derived from mitochondrial DNA of patients with nonfamilial Alzheimer's disease suggests an even broader implication for the neuroprotective role of dopamine agonists. Although the clinical evidence for neuroprotection by dopamine agonists is still limited, the preliminary results from several ongoing clinical trials are promising. Several longitudinal studies are currently in progress designed to demonstrate a delay or slowing of progression of Parkinson's disease using various surrogate markers of neuronal degeneration such as 18F-levodopa positron emission tomography and 123I beta-CIT (carbomethoxy-beta-4-iodophenyl-nortropane) single positron emission computed tomography. The results of these experimental and clinical studies will improve our understanding of the action of dopamine agonists and provide critical information needed for planning future therapeutic strategies for Parkinson's disease and related neurodegenerative disorders.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Le</LastName><ForeName>W D</ForeName><Initials>WD</Initials><AffiliationInfo><Affiliation>Department of Neurology, Baylor College of Medicine, Houston, Texas 77030, USA. 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