Symptomatic Models of Parkinson's Disease and L-DOPA-Induced Dyskinesia in Non-human Primates.
Identifieur interne : 000522 ( Main/Exploration ); précédent : 000521; suivant : 000523Symptomatic Models of Parkinson's Disease and L-DOPA-Induced Dyskinesia in Non-human Primates.
Auteurs : Tom M. Johnston [Canada] ; Susan H. FoxSource :
- Current topics in behavioral neurosciences [ 1866-3370 ] ; 2015.
English descriptors
- KwdEn :
- MESH :
- chemical , pharmacology : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Dopamine Agents, Levodopa.
- therapy : Parkinson Disease.
- Animals, Disease Models, Animal, Dyskinesia, Drug-Induced, Humans, Primates.
Abstract
Models of Parkinson's disease (PD) can be produced in several non-human primate (NHP) species by applying neurotoxic lesions to the nigrostriatal dopamine pathway. The most commonly used neurotoxin is MPTP, a compound accidentally discovered as a contaminant of street drugs. Compared to other neurotoxins, MPTP has the advantage of crossing the blood-brain barrier and can thus be administered systemically. MPTP-lesioned NHPs exhibit the main core clinical features of PD. When treated with L-DOPA, these NHP models develop involuntary movements resembling the phenomenology of human dyskinesias. In old-world NHP species (macaques, baboons), choreic and dystonic dyskinesias can be readily distinguished and quantified with specific rating scales. More recently, certain non-motor symptoms relevant to human PD have been described in L-DOPA-treated MPTP-NHPs, including a range of neuropsychiatric abnormalities and sleep disturbances. The main shortcomings of MPTP-NHP models consist in a lack of progression of the underlying neurodegenerative lesion, along with an inability to model the intracellular protein-inclusion pathology typical of PD. The strength of MPTP-NHP models lies in their face and predictive validity for symptomatic treatments of parkinsonian motor features. Indeed, these models have been instrumental to the development of several medical and surgical approaches that are currently applied to treat PD.
DOI: 10.1007/7854_2014_352
PubMed: 25158623
Affiliations:
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Le document en format XML
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Johnston</name><affiliation wicri:level="4"><nlm:affiliation>Toronto Western Research Institute, University of Toronto, Toronto Western Hospital, 399, Bathurst St, Toronto, ON, M5T 2S8, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Toronto Western Research Institute, University of Toronto, Toronto Western Hospital, 399, Bathurst St, Toronto, ON, M5T 2S8</wicri:regionArea><orgName type="university">Université de Toronto</orgName><placeName><settlement type="city">Toronto</settlement><region type="state">Ontario</region></placeName></affiliation></author><author><name sortKey="Fox, Susan H" sort="Fox, Susan H" uniqKey="Fox S" first="Susan H" last="Fox">Susan H. Fox</name></author></analytic><series><title level="j">Current topics in behavioral neurosciences</title><idno type="ISSN">1866-3370</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (pharmacology)</term><term>Animals</term><term>Disease Models, Animal</term><term>Dopamine Agents (pharmacology)</term><term>Dyskinesia, Drug-Induced</term><term>Humans</term><term>Levodopa (pharmacology)</term><term>Parkinson Disease (therapy)</term><term>Primates</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term><term>Dopamine Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Dyskinesia, Drug-Induced</term><term>Humans</term><term>Primates</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Models of Parkinson's disease (PD) can be produced in several non-human primate (NHP) species by applying neurotoxic lesions to the nigrostriatal dopamine pathway. The most commonly used neurotoxin is MPTP, a compound accidentally discovered as a contaminant of street drugs. Compared to other neurotoxins, MPTP has the advantage of crossing the blood-brain barrier and can thus be administered systemically. MPTP-lesioned NHPs exhibit the main core clinical features of PD. When treated with L-DOPA, these NHP models develop involuntary movements resembling the phenomenology of human dyskinesias. In old-world NHP species (macaques, baboons), choreic and dystonic dyskinesias can be readily distinguished and quantified with specific rating scales. More recently, certain non-motor symptoms relevant to human PD have been described in L-DOPA-treated MPTP-NHPs, including a range of neuropsychiatric abnormalities and sleep disturbances. The main shortcomings of MPTP-NHP models consist in a lack of progression of the underlying neurodegenerative lesion, along with an inability to model the intracellular protein-inclusion pathology typical of PD. The strength of MPTP-NHP models lies in their face and predictive validity for symptomatic treatments of parkinsonian motor features. Indeed, these models have been instrumental to the development of several medical and surgical approaches that are currently applied to treat PD.</div></front></TEI><affiliations><list><country><li>Canada</li></country><region><li>Ontario</li></region><settlement><li>Toronto</li></settlement><orgName><li>Université de Toronto</li></orgName></list><tree><noCountry><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"><region name="Ontario"><name sortKey="Johnston, Tom M" sort="Johnston, Tom M" uniqKey="Johnston T" first="Tom M" last="Johnston">Tom M. Johnston</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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