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La maladie de Parkinson au Canada (serveur d'exploration)

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Modeling dyskinesia in animal models of Parkinson disease : ANIMAL MODELS OF PARKINSON'S DISEASE

Identifieur interne : 000C00 ( PascalFrancis/Curation ); précédent : 000B99; suivant : 000C01

Modeling dyskinesia in animal models of Parkinson disease : ANIMAL MODELS OF PARKINSON'S DISEASE

Auteurs : Nicolas Morin [Canada] ; Vincent A. Jourdain ; Thérèse Di Paolo

Source :

RBID : Pascal:14-0182393

Descripteurs français

English descriptors

Abstract

The treatment of motor symptoms of Parkinson disease (PD) with the dopamine (DA) precursor, L-3,4-dihydroxyphenylalanine (L-DOPA) introduced 50 years ago still remains a very effective medication. However, involuntary movements termed L-DOPA-induced dyskinesias (LID) appear in the vast majority of PD patients after chronic treatment and may become disabling. Once they appeared, the first dose after a several-weeks drug holiday will trigger them again, showing that L-DOPA has permanently or persistently modified the brain response to DA. LID are very difficult to manage and no drug is yet approved for dyskinesias, aside from a modest benefit with amantadine. New drugs are needed for PD to alleviate parkinsonian symptoms without inducing dyskinesias. Hence, animal models have been developed to seek the mechanisms involved in LID and new drug targets. The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was discovered as a contamination of a derivative of heroin taken by drug users and produced similar motor symptoms as idiopathic PD. Since then, MPTP is used extensively to model PD and LID in non-human primates and mice in addition to the classical PD model in rats with a 6-hydroxydopamine (6-OHDA) lesion. This article reviews rodent and non-human primate models of PD that reproduce motor complications induced by DA replacement therapy. Moreover, key biochemical changes in the brain of post-mortem PD patients with LID will be compared to those observed in animal models. Finally, the translational usefulness of drugs found to treat LID in animal models will be compared to their clinical activities.
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A08 01  1  ENG  @1 Modeling dyskinesia in animal models of Parkinson disease : ANIMAL MODELS OF PARKINSON'S DISEASE
A11 01  1    @1 MORIN (Nicolas)
A11 02  1    @1 JOURDAIN (Vincent A.)
A11 03  1    @1 DI PAOLO (Thérèse)
A14 01      @1 Neuroscience Research Unit, Centre de recherche du CHU de Québec @2 Quebec (QC) @3 CAN
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C01 01    ENG  @0 The treatment of motor symptoms of Parkinson disease (PD) with the dopamine (DA) precursor, L-3,4-dihydroxyphenylalanine (L-DOPA) introduced 50 years ago still remains a very effective medication. However, involuntary movements termed L-DOPA-induced dyskinesias (LID) appear in the vast majority of PD patients after chronic treatment and may become disabling. Once they appeared, the first dose after a several-weeks drug holiday will trigger them again, showing that L-DOPA has permanently or persistently modified the brain response to DA. LID are very difficult to manage and no drug is yet approved for dyskinesias, aside from a modest benefit with amantadine. New drugs are needed for PD to alleviate parkinsonian symptoms without inducing dyskinesias. Hence, animal models have been developed to seek the mechanisms involved in LID and new drug targets. The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was discovered as a contamination of a derivative of heroin taken by drug users and produced similar motor symptoms as idiopathic PD. Since then, MPTP is used extensively to model PD and LID in non-human primates and mice in addition to the classical PD model in rats with a 6-hydroxydopamine (6-OHDA) lesion. This article reviews rodent and non-human primate models of PD that reproduce motor complications induced by DA replacement therapy. Moreover, key biochemical changes in the brain of post-mortem PD patients with LID will be compared to those observed in animal models. Finally, the translational usefulness of drugs found to treat LID in animal models will be compared to their clinical activities.
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C03 01  X  FRE  @0 Dyskinésie @5 01
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C03 01  X  SPA  @0 Disquinesia @5 01
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C03 02  X  SPA  @0 Parkinson enfermedad @2 NM @5 02
C03 03  X  FRE  @0 Mouvement involontaire @5 03
C03 03  X  ENG  @0 Involuntary movement @5 03
C03 03  X  SPA  @0 Movimiento involuntario @5 03
C03 04  X  FRE  @0 Pathologie du système nerveux @5 04
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C03 06  X  ENG  @0 Animal model @5 10
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C03 07  X  FRE  @0 Lévodopa @2 NK @2 FR @5 11
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C03 08  X  SPA  @0 Primates @2 NS @5 12
C03 09  X  FRE  @0 Rodentia @2 NS @5 13
C03 09  X  ENG  @0 Rodentia @2 NS @5 13
C03 09  X  SPA  @0 Rodentia @2 NS @5 13
C03 10  X  FRE  @0 Animal @5 14
C03 10  X  ENG  @0 Animal @5 14
C03 10  X  SPA  @0 Animal @5 14
C03 11  X  FRE  @0 Mouvement anormal @5 15
C03 11  X  ENG  @0 Abnormal movement @5 15
C03 11  X  SPA  @0 Movimiento anormal @5 15
C03 12  X  FRE  @0 Complication @5 16
C03 12  X  ENG  @0 Complication @5 16
C03 12  X  SPA  @0 Complicación @5 16
C07 01  X  FRE  @0 Mammalia @2 NS
C07 01  X  ENG  @0 Mammalia @2 NS
C07 01  X  SPA  @0 Mammalia @2 NS
C07 02  X  FRE  @0 Vertebrata @2 NS
C07 02  X  ENG  @0 Vertebrata @2 NS
C07 02  X  SPA  @0 Vertebrata @2 NS
C07 03  X  FRE  @0 Syndrome extrapyramidal @5 37
C07 03  X  ENG  @0 Extrapyramidal syndrome @5 37
C07 03  X  SPA  @0 Extrapiramidal síndrome @5 37
C07 04  X  FRE  @0 Trouble neurologique @5 39
C07 04  X  ENG  @0 Neurological disorder @5 39
C07 04  X  SPA  @0 Trastorno neurológico @5 39
C07 05  X  FRE  @0 Pathologie de l'encéphale @5 40
C07 05  X  ENG  @0 Cerebral disorder @5 40
C07 05  X  SPA  @0 Encéfalo patología @5 40
C07 06  X  FRE  @0 Maladie dégénérative @5 41
C07 06  X  ENG  @0 Degenerative disease @5 41
C07 06  X  SPA  @0 Enfermedad degenerativa @5 41
C07 07  X  FRE  @0 Pathologie du système nerveux central @5 42
C07 07  X  ENG  @0 Central nervous system disease @5 42
C07 07  X  SPA  @0 Sistema nervosio central patología @5 42
N21       @1 230
N44 01      @1 OTO
N82       @1 OTO

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Le document en format XML

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<s0>Complication</s0>
<s5>16</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG">
<s0>Complication</s0>
<s5>16</s5>
</fC03>
<fC03 i1="12" i2="X" l="SPA">
<s0>Complicación</s0>
<s5>16</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Syndrome extrapyramidal</s0>
<s5>37</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Extrapyramidal syndrome</s0>
<s5>37</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Extrapiramidal síndrome</s0>
<s5>37</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Trouble neurologique</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Neurological disorder</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Trastorno neurológico</s0>
<s5>39</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Pathologie de l'encéphale</s0>
<s5>40</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Cerebral disorder</s0>
<s5>40</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Encéfalo patología</s0>
<s5>40</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE">
<s0>Maladie dégénérative</s0>
<s5>41</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG">
<s0>Degenerative disease</s0>
<s5>41</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA">
<s0>Enfermedad degenerativa</s0>
<s5>41</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE">
<s0>Pathologie du système nerveux central</s0>
<s5>42</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG">
<s0>Central nervous system disease</s0>
<s5>42</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA">
<s0>Sistema nervosio central patología</s0>
<s5>42</s5>
</fC07>
<fN21>
<s1>230</s1>
</fN21>
<fN44 i1="01">
<s1>OTO</s1>
</fN44>
<fN82>
<s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
</record>

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