Permeability of blood-brain barrier in macaque model of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson disease.
Identifieur interne : 001928 ( Ncbi/Curation ); précédent : 001927; suivant : 001929Permeability of blood-brain barrier in macaque model of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson disease.
Auteurs : Thibaud Thiollier [France] ; Caisheng Wu ; Hugues Contamin [France] ; Qin Li [Royaume-Uni] ; Jinlan Zhang ; Erwan Bezard [France]Source :
- Synapse (New York, N.Y.) [ 1098-2396 ] ; 2016.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (pharmacology), Animals, Blood-Brain Barrier (drug effects), Brain (drug effects), Disease Models, Animal, Dopamine (metabolism), Levodopa (pharmacology), Macaca, Male, Parkinson Disease (drug therapy), Parkinson Disease, Secondary (chemically induced), Permeability (drug effects), Pyridines (pharmacology).
- MESH :
- chemical , metabolism : Dopamine.
- chemical , pharmacology : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Levodopa, Pyridines.
- chemically induced : Parkinson Disease, Secondary.
- drug effects : Blood-Brain Barrier, Brain, Permeability.
- drug therapy : Parkinson Disease.
- Animals, Disease Models, Animal, Macaca, Male.
Abstract
Brain bioavailability of drugs developed to address central nervous system diseases is classically documented through cerebrospinal fluid collected in normal animals, i.e., through an approximation as there are fundamental differences between cerebrospinal fluid and tissue contents. The fact that disease might affect brain availability of drugs is almost never considered at this stage although several conditions are associated with blood-brain barrier damage. Building upon our expertise in Parkinson's disease translational research, the present study addressed this gap comparing plasma and cerebrospinal fluid bioavailability of l-3,4-dihydroxyphenylalanine, carbamazepine, quinidine, lovastatin, and simvastatin, in healthy and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated macaques, the gold standard model of Parkinson's disease. The drugs were selected based upon their differential transport across the blood-brain barrier. Interestingly, brain bioavailability of quinidine was decreased while others were unaffected. Pharmacokinetics and pharmacodynamics experiments of drugs addressing Parkinson's disease might thus be performed in healthy animals unless the drugs are known to interact with the organic cation transporter.
DOI: 10.1002/syn.21889
PubMed: 26799359
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Caisheng Wu<affiliation><nlm:affiliation>Institute of Materia Medica, Chinese Academy of Medical Sciences, Beijing, People's Republic of China, 100050.</nlm:affiliation><wicri:noCountry code="subField">100050</wicri:noCountry></affiliation><affiliation><nlm:affiliation>Institute of Materia Medica, Chinese Academy of Medical Sciences, Beijing, People's Republic of China, 100050.</nlm:affiliation><wicri:noCountry code="subField">100050</wicri:noCountry></affiliation>Le document en format XML
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induced" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Blood-Brain Barrier</term><term>Brain</term><term>Permeability</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Macaca</term><term>Male</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Brain bioavailability of drugs developed to address central nervous system diseases is classically documented through cerebrospinal fluid collected in normal animals, i.e., through an approximation as there are fundamental differences between cerebrospinal fluid and tissue contents. The fact that disease might affect brain availability of drugs is almost never considered at this stage although several conditions are associated with blood-brain barrier damage. Building upon our expertise in Parkinson's disease translational research, the present study addressed this gap comparing plasma and cerebrospinal fluid bioavailability of l-3,4-dihydroxyphenylalanine, carbamazepine, quinidine, lovastatin, and simvastatin, in healthy and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated macaques, the gold standard model of Parkinson's disease. The drugs were selected based upon their differential transport across the blood-brain barrier. Interestingly, brain bioavailability of quinidine was decreased while others were unaffected. Pharmacokinetics and pharmacodynamics experiments of drugs addressing Parkinson's disease might thus be performed in healthy animals unless the drugs are known to interact with the organic cation transporter.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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