Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/23134
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dc.contributor.authorBlanchet, P. J.en
dc.contributor.authorKonitsiotis, S.en
dc.contributor.authorHyland, K.en
dc.contributor.authorArnold, L. A.en
dc.contributor.authorPettigrew, K. D.en
dc.contributor.authorChase, T. N.en
dc.date.accessioned2015-11-24T19:30:37Z-
dc.date.available2015-11-24T19:30:37Z-
dc.identifier.issn0014-4886-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/23134-
dc.rightsDefault Licence-
dc.subject*1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridineen
dc.subject3,4-Dihydroxyphenylacetic Acid/cerebrospinal fluiden
dc.subjectAnimalsen
dc.subjectBiological Markers/cerebrospinal fluiden
dc.subjectBiopterin/analogs & derivatives/cerebrospinal fluiden
dc.subjectDisease Models, Animalen
dc.subjectFemaleen
dc.subjectFree Radical Scavengers/blood/*pharmacologyen
dc.subjectHomovanillic Acid/cerebrospinal fluiden
dc.subjectIndans/blood/*pharmacologyen
dc.subjectMacaca fascicularisen
dc.subjectMaleen
dc.subjectMethoxyhydroxyphenylglycol/cerebrospinal fluiden
dc.subjectMotor Activity/*drug effectsen
dc.subjectParkinson Disease, Secondary/cerebrospinal fluid/*physiopathologyen
dc.subjectPilot Projectsen
dc.subjectPiperazines/blood/*pharmacologyen
dc.titleChronic exposure to MPTP as a primate model of progressive parkinsonism: a pilot study with a free radical scavengeren
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.primary10.1006/exnr.1998.6906-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/9784281-
heal.identifier.secondaryhttp://ac.els-cdn.com/S0014488698969060/1-s2.0-S0014488698969060-main.pdf?_tid=353e24eab08438225fcaaa2099f4c529&acdnat=1332840441_a041f68a49d4e0e1ad97d7044a9c9704-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate1998-
heal.abstractThe development of a validated primate model of progressive parkinsonism is a critical step in the evaluation of drugs that might halt or slow progression of Parkinson's disease. In this pilot study, we gradually exposed 14 cynomolgus monkeys to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), at a weekly dose of 0.5 mg/kg s.c. for 10 weeks, to determine their probability of not reaching a predetermined endpoint on a disability scale by Kaplan-Meier analysis. Four other MPTP-exposed animals were coadministered the potent free radical scavenger 7-hydroxy-1-[4-(3-methoxyphenyl)-1-piperazinyl]acetylamino-2,2,4,6- tetramethylindan (OPC-14117) as a single oral daily dose of 0.6 g/kg, starting 2 weeks before MPTP initiation. The risk of reaching endpoint by week 10 was 79% and mean time before reaching endpoint was 6 weeks. Global motor activity, recorded in a subset of animals using a portable activity monitor, declined following the first MPTP dose and never recovered. Several cerebrospinal fluid indices of central monoamine metabolism collected by suboccipital puncture at 0, 5, and 10 weeks, including HVA, DOPAC, and tetrahydrobiopterin but not MHPG, were found to be "trait" markers for MPTP exposure, whereas CSF DOPAC and tetrahydrobiopterin constituted potential "state" markers for reaching endpoint. The antioxidant OPC-14117 did not protect against MPTP-induced parkinsonism. Further attempts to validate this incremental model of neurotoxin-induced parkinsonism as a predictor of patient responses to putative neuroprotective agents appear warranted.en
heal.journalNameExp Neurolen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ

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