N-methylation underlying Parkinson's disease
Identifieur interne :
001023 ( PascalFrancis/Corpus );
précédent :
001022;
suivant :
001024
N-methylation underlying Parkinson's disease
Auteurs : Kazuo Matsubara ;
Koji Aoyama ;
Manabu Suno ;
Toshio AwayaSource :
-
Neurotoxicology and teratology [ 0892-0362 ] ; 2002.
RBID : Pascal:03-0018075
Descripteurs français
English descriptors
Abstract
The discovery of 1-methyl-4-phenyl-1,2,2,6-tetrahydropyridine (MPTP) leads to the hypothesis that Parkinson's disease (PD) is may be initiated or precipitated by environmental or endogenous toxins by the mechanism similar to that of MPTP in genetically-predisposed individuals. Endogenous analogs of MPTP, such as β-carbolines (βCs) and tetrahydroisoquinolines, have been proposed as possible causative candidates causing PD and are bioactivated into potential neurotoxins by N-methylation enzyme(s). These N-methylated βCs and tetrahydroisoquinoline have been higher cerebrospinal levels in parkinsonian patients than age-matched controls. Thus, there is a hypotheses to influence the pathogenesis of PD, that is, the excess enzyme activity to activate neurotoxins, such as N-methyltransferase, might be higher in PDs. Indeed, simple βCs, via N-methylation steps, induced bradykinesia with the decreased dopamine contents in the striatum and midbrain in C57/BL mice. In younger (65 years old) PD patients, the excretion amount of N1-methyl-nicotinamaide was significantly higher than that in younger controls. The protein amount of nicotinamide N-methyltransferase (NNMT) was also significantly higher in younger PD patients than that in younger controls. These findings described here would indicate that the excess N-methylation ability for azaheterocyclic amines, such as βCs, before the onset had been implicated in PD pathogenesis. On the other hand, the contribution of aberrant cytochrome P450 or aldehyde oxidase activity acting on the pyridine ring, that could act as detoxification routes of endogenous neurotoxins, would be small in the etiology of PD.
Notice en format standard (ISO 2709)
Pour connaître la documentation sur le format Inist Standard.
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| A01 | 01 | 1 | | @0 0892-0362 |
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| A02 | 01 | | | @0 NETEEC |
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| A03 | | 1 | | @0 Neurotoxicol. teratol. |
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| A05 | | | | @2 24 |
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| A06 | | | | @2 5 |
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| A08 | 01 | 1 | ENG | @1 N-methylation underlying Parkinson's disease |
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| A09 | 01 | 1 | ENG | @1 Milestones in Research on Neurotoxins and Neuroprotection: A Tribute to Professor Toshiharu Nagatsu |
|---|
| A11 | 01 | 1 | | @1 MATSUBARA (Kazuo) |
|---|
| A11 | 02 | 1 | | @1 AOYAMA (Koji) |
|---|
| A11 | 03 | 1 | | @1 SUNO (Manabu) |
|---|
| A11 | 04 | 1 | | @1 AWAYA (Toshio) |
|---|
| A12 | 01 | 1 | | @1 NAOI (Makoto) @9 ed. |
|---|
| A12 | 02 | 1 | | @1 PARVEZ (Hasan) @9 ed. |
|---|
| A12 | 03 | 1 | | @1 MARUYAMA (Wakako) @9 ed. |
|---|
| A12 | 04 | 1 | | @1 COLLINS (Michel A.) @9 ed. |
|---|
| A12 | 05 | 1 | | @1 YOUDIM (Moussa B. H.) @9 ed. |
|---|
| A14 | 01 | | | @1 Department of Hospital Pharmacy and Pharmacology, Asahikawa Medical College @2 Asahikawa 078-8510 @3 JPN @Z 1 aut. @Z 3 aut. @Z 4 aut. |
|---|
| A14 | 02 | | | @1 Department of Internal Medicine III, Shimane Medical University @2 Izumo 693-8501 @3 JPN @Z 2 aut. |
|---|
| A15 | 01 | | | @1 Department of Brain Sciences, Institute of Applied Biochemistry, Yagi Memorial Park @2 Mitake, Gifu 505-0116 @3 JPN @Z 1 aut. |
|---|
| A15 | 02 | | | @1 Unit of Neuroendocrinology, Bat. 5, Parc Chateau, CNRS @2 91190 Gif sur Yvette @3 FRA @Z 2 aut. |
|---|
| A15 | 03 | | | @1 Laboratory of Biochemistry and Metabolism, Department of Basic Gerontology, National Institute of Longevity Sciences @2 Obu, Aichi 474-8622 @3 JPN @Z 3 aut. |
|---|
| A15 | 04 | | | @1 Department of Molecular and Cellular Biochemistry, Loyola University of Chicago, Strich School of Medicine @2 Maywood, IL 60153 @3 USA @Z 4 aut. |
|---|
| A15 | 05 | | | @1 Eve Topf and National Parkinson Foundation Neurodegenerative Diseases Centers, Department of Pharmacology, Rappaport Faculty of Medicine, Technion @2 Haifa 31096 @3 ISR @Z 5 aut. |
|---|
| A20 | | | | @1 593-598 |
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| A21 | | | | @1 2002 |
|---|
| A23 | 01 | | | @0 ENG |
|---|
| A43 | 01 | | | @1 INIST @2 18910 @5 354000109244300040 |
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| A44 | | | | @0 0000 @1 © 2003 INIST-CNRS. All rights reserved. |
|---|
| A45 | | | | @0 32 ref. |
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| A47 | 01 | 1 | | @0 03-0018075 |
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| A60 | | | | @1 P @2 C |
|---|
| A61 | | | | @0 A |
|---|
| A64 | 01 | 1 | | @0 Neurotoxicology and teratology |
|---|
| A66 | 01 | | | @0 USA |
|---|
| C01 | 01 | | ENG | @0 The discovery of 1-methyl-4-phenyl-1,2,2,6-tetrahydropyridine (MPTP) leads to the hypothesis that Parkinson's disease (PD) is may be initiated or precipitated by environmental or endogenous toxins by the mechanism similar to that of MPTP in genetically-predisposed individuals. Endogenous analogs of MPTP, such as β-carbolines (βCs) and tetrahydroisoquinolines, have been proposed as possible causative candidates causing PD and are bioactivated into potential neurotoxins by N-methylation enzyme(s). These N-methylated βCs and tetrahydroisoquinoline have been higher cerebrospinal levels in parkinsonian patients than age-matched controls. Thus, there is a hypotheses to influence the pathogenesis of PD, that is, the excess enzyme activity to activate neurotoxins, such as N-methyltransferase, might be higher in PDs. Indeed, simple βCs, via N-methylation steps, induced bradykinesia with the decreased dopamine contents in the striatum and midbrain in C57/BL mice. In younger (65 years old) PD patients, the excretion amount of N1-methyl-nicotinamaide was significantly higher than that in younger controls. The protein amount of nicotinamide N-methyltransferase (NNMT) was also significantly higher in younger PD patients than that in younger controls. These findings described here would indicate that the excess N-methylation ability for azaheterocyclic amines, such as βCs, before the onset had been implicated in PD pathogenesis. On the other hand, the contribution of aberrant cytochrome P450 or aldehyde oxidase activity acting on the pyridine ring, that could act as detoxification routes of endogenous neurotoxins, would be small in the etiology of PD. |
|---|
| C02 | 01 | X | | @0 002B17G |
|---|
| C03 | 01 | X | FRE | @0 Carboline dérivé @2 FR @5 01 |
|---|
| C03 | 01 | X | ENG | @0 Carboline derivatives @2 FR @5 01 |
|---|
| C03 | 02 | X | FRE | @0 Toxicité @5 04 |
|---|
| C03 | 02 | X | ENG | @0 Toxicity @5 04 |
|---|
| C03 | 02 | X | SPA | @0 Toxicidad @5 04 |
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| C03 | 03 | X | FRE | @0 Méthylation @5 07 |
|---|
| C03 | 03 | X | ENG | @0 Methylation @5 07 |
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| C03 | 03 | X | SPA | @0 Metilación @5 07 |
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| C03 | 04 | X | FRE | @0 Parkinson maladie @5 10 |
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| C03 | 04 | X | ENG | @0 Parkinson disease @5 10 |
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| C03 | 04 | X | SPA | @0 Parkinson enfermedad @5 10 |
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| C03 | 05 | X | FRE | @0 Etiologie @5 11 |
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| C03 | 05 | X | ENG | @0 Etiology @5 11 |
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| C03 | 05 | X | SPA | @0 Etiología @5 11 |
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| C03 | 06 | X | FRE | @0 Pathogénie @5 12 |
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| C03 | 06 | X | ENG | @0 Pathogenesis @5 12 |
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| C03 | 06 | X | SPA | @0 Patogenia @5 12 |
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| C03 | 07 | X | FRE | @0 Homme @5 13 |
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| C03 | 07 | X | ENG | @0 Human @5 13 |
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| C07 | 01 | X | FRE | @0 Système nerveux pathologie @5 61 |
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| C07 | 01 | X | ENG | @0 Nervous system diseases @5 61 |
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| C07 | 01 | X | SPA | @0 Sistema nervioso patología @5 61 |
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| C07 | 02 | X | FRE | @0 Système nerveux central pathologie @5 62 |
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| C07 | 02 | X | ENG | @0 Central nervous system disease @5 62 |
|---|
| C07 | 02 | X | SPA | @0 Sistema nervosio central patología @5 62 |
|---|
| C07 | 03 | X | FRE | @0 Encéphale pathologie @5 63 |
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| C07 | 03 | X | ENG | @0 Cerebral disorder @5 63 |
|---|
| C07 | 03 | X | SPA | @0 Encéfalo patología @5 63 |
|---|
| C07 | 04 | X | FRE | @0 Extrapyramidal syndrome @5 64 |
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| C07 | 04 | X | ENG | @0 Extrapyramidal syndrome @5 64 |
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| C07 | 04 | X | SPA | @0 Extrapiramidal síndrome @5 64 |
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| C07 | 05 | X | FRE | @0 Maladie dégénérative @5 65 |
|---|
| C07 | 05 | X | ENG | @0 Degenerative disease @5 65 |
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| C07 | 05 | X | SPA | @0 Enfermedad degenerativa @5 65 |
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| N21 | | | | @1 006 |
|---|
| N82 | | | | @1 PSI |
|---|
|
|---|
| pR |
| A30 | 01 | 1 | ENG | @1 International Catecholamine Symposium @2 9 @3 Kyoto JPN @4 2001-03-31 |
|---|
| A30 | 02 | 1 | ENG | @1 International Joint Congresses on Progress in Alzheimer's and Parkinson's Disease @2 5 @3 Kyoto JPN @4 2001-03-31 |
|---|
|
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Format Inist (serveur)
| NO : | PASCAL 03-0018075 INIST |
|---|
| ET : | N-methylation underlying Parkinson's disease |
|---|
| AU : | MATSUBARA (Kazuo); AOYAMA (Koji); SUNO (Manabu); AWAYA (Toshio); NAOI (Makoto); PARVEZ (Hasan); MARUYAMA (Wakako); COLLINS (Michel A.); YOUDIM (Moussa B. H.) |
|---|
| AF : | Department of Hospital Pharmacy and Pharmacology, Asahikawa Medical College/Asahikawa 078-8510/Japon (1 aut., 3 aut., 4 aut.); Department of Internal Medicine III, Shimane Medical University/Izumo 693-8501/Japon (2 aut.); Department of Brain Sciences, Institute of Applied Biochemistry, Yagi Memorial Park/Mitake, Gifu 505-0116/Japon (1 aut.); Unit of Neuroendocrinology, Bat. 5, Parc Chateau, CNRS/91190 Gif sur Yvette/France (2 aut.); Laboratory of Biochemistry and Metabolism, Department of Basic Gerontology, National Institute of Longevity Sciences/Obu, Aichi 474-8622/Japon (3 aut.); Department of Molecular and Cellular Biochemistry, Loyola University of Chicago, Strich School of Medicine/Maywood, IL 60153/Etats-Unis (4 aut.); Eve Topf and National Parkinson Foundation Neurodegenerative Diseases Centers, Department of Pharmacology, Rappaport Faculty of Medicine, Technion/Haifa 31096/Israël (5 aut.) |
|---|
| DT : | Publication en série; Congrès; Niveau analytique |
|---|
| SO : | Neurotoxicology and teratology; ISSN 0892-0362; Coden NETEEC; Etats-Unis; Da. 2002; Vol. 24; No. 5; Pp. 593-598; Bibl. 32 ref. |
|---|
| LA : | Anglais |
|---|
| EA : | The discovery of 1-methyl-4-phenyl-1,2,2,6-tetrahydropyridine (MPTP) leads to the hypothesis that Parkinson's disease (PD) is may be initiated or precipitated by environmental or endogenous toxins by the mechanism similar to that of MPTP in genetically-predisposed individuals. Endogenous analogs of MPTP, such as β-carbolines (βCs) and tetrahydroisoquinolines, have been proposed as possible causative candidates causing PD and are bioactivated into potential neurotoxins by N-methylation enzyme(s). These N-methylated βCs and tetrahydroisoquinoline have been higher cerebrospinal levels in parkinsonian patients than age-matched controls. Thus, there is a hypotheses to influence the pathogenesis of PD, that is, the excess enzyme activity to activate neurotoxins, such as N-methyltransferase, might be higher in PDs. Indeed, simple βCs, via N-methylation steps, induced bradykinesia with the decreased dopamine contents in the striatum and midbrain in C57/BL mice. In younger (65 years old) PD patients, the excretion amount of N1-methyl-nicotinamaide was significantly higher than that in younger controls. The protein amount of nicotinamide N-methyltransferase (NNMT) was also significantly higher in younger PD patients than that in younger controls. These findings described here would indicate that the excess N-methylation ability for azaheterocyclic amines, such as βCs, before the onset had been implicated in PD pathogenesis. On the other hand, the contribution of aberrant cytochrome P450 or aldehyde oxidase activity acting on the pyridine ring, that could act as detoxification routes of endogenous neurotoxins, would be small in the etiology of PD. |
|---|
| CC : | 002B17G |
|---|
| FD : | Carboline dérivé; Toxicité; Méthylation; Parkinson maladie; Etiologie; Pathogénie; Homme |
|---|
| FG : | Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative |
|---|
| ED : | Carboline derivatives; Toxicity; Methylation; Parkinson disease; Etiology; Pathogenesis; Human |
|---|
| EG : | Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease |
|---|
| SD : | Toxicidad; Metilación; Parkinson enfermedad; Etiología; Patogenia; Hombre |
|---|
| LO : | INIST-18910.354000109244300040 |
|---|
| ID : | 03-0018075 |
|---|
Links to Exploration step
Pascal:03-0018075
Le document en format XML
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</inist:fA14><author><name sortKey="Suno, Manabu" sort="Suno, Manabu" uniqKey="Suno M" first="Manabu" last="Suno">Manabu Suno</name>
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</inist:fA14><series><title level="j" type="main">Neurotoxicology and teratology</title>
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<idno type="ISSN">0892-0362</idno>
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</imprint><seriesStmt><title level="j" type="main">Neurotoxicology and teratology</title>
<title level="j" type="abbreviated">Neurotoxicol. teratol.</title>
<idno type="ISSN">0892-0362</idno>
</seriesStmt><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Carboline derivatives</term>
<term>Etiology</term>
<term>Human</term>
<term>Methylation</term>
<term>Parkinson disease</term>
<term>Pathogenesis</term>
<term>Toxicity</term>
</keywords><keywords scheme="Pascal" xml:lang="fr"><term>Carboline dérivé</term>
<term>Toxicité</term>
<term>Méthylation</term>
<term>Parkinson maladie</term>
<term>Etiologie</term>
<term>Pathogénie</term>
<term>Homme</term>
</keywords><front><div type="abstract" xml:lang="en">The discovery of 1-methyl-4-phenyl-1,2,2,6-tetrahydropyridine (MPTP) leads to the hypothesis that Parkinson's disease (PD) is may be initiated or precipitated by environmental or endogenous toxins by the mechanism similar to that of MPTP in genetically-predisposed individuals. Endogenous analogs of MPTP, such as β-carbolines (βCs) and tetrahydroisoquinolines, have been proposed as possible causative candidates causing PD and are bioactivated into potential neurotoxins by N-methylation enzyme(s). These N-methylated βCs and tetrahydroisoquinoline have been higher cerebrospinal levels in parkinsonian patients than age-matched controls. Thus, there is a hypotheses to influence the pathogenesis of PD, that is, the excess enzyme activity to activate neurotoxins, such as N-methyltransferase, might be higher in PDs. Indeed, simple βCs, via N-methylation steps, induced bradykinesia with the decreased dopamine contents in the striatum and midbrain in C57/BL mice. In younger (65 years old) PD patients, the excretion amount of N<sup>1</sup>
-methyl-nicotinamaide was significantly higher than that in younger controls. The protein amount of nicotinamide N-methyltransferase (NNMT) was also significantly higher in younger PD patients than that in younger controls. These findings described here would indicate that the excess N-methylation ability for azaheterocyclic amines, such as βCs, before the onset had been implicated in PD pathogenesis. On the other hand, the contribution of aberrant cytochrome P450 or aldehyde oxidase activity acting on the pyridine ring, that could act as detoxification routes of endogenous neurotoxins, would be small in the etiology of PD.</div><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0892-0362</s0>
</fA01><fA02 i1="01"><s0>NETEEC</s0>
</fA02><fA03 i2="1"><s0>Neurotoxicol. teratol.</s0>
</fA03><fA08 i1="01" i2="1" l="ENG"><s1>N-methylation underlying Parkinson's disease</s1>
</fA08><fA09 i1="01" i2="1" l="ENG"><s1>Milestones in Research on Neurotoxins and Neuroprotection: A Tribute to Professor Toshiharu Nagatsu</s1>
</fA09><fA11 i1="01" i2="1"><s1>MATSUBARA (Kazuo)</s1>
</fA11><fA11 i1="02" i2="1"><s1>AOYAMA (Koji)</s1>
</fA11><fA11 i1="03" i2="1"><s1>SUNO (Manabu)</s1>
</fA11><fA11 i1="04" i2="1"><s1>AWAYA (Toshio)</s1>
</fA11><fA12 i1="01" i2="1"><s1>NAOI (Makoto)</s1>
<s9>ed.</s9>
</fA12><fA12 i1="02" i2="1"><s1>PARVEZ (Hasan)</s1>
<s9>ed.</s9>
</fA12><fA12 i1="03" i2="1"><s1>MARUYAMA (Wakako)</s1>
<s9>ed.</s9>
</fA12><fA12 i1="04" i2="1"><s1>COLLINS (Michel A.)</s1>
<s9>ed.</s9>
</fA12><fA12 i1="05" i2="1"><s1>YOUDIM (Moussa B. H.)</s1>
<s9>ed.</s9>
</fA12><fA14 i1="01"><s1>Department of Hospital Pharmacy and Pharmacology, Asahikawa Medical College</s1>
<s2>Asahikawa 078-8510</s2>
<s3>JPN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
</fA14><fA14 i1="02"><s1>Department of Internal Medicine III, Shimane Medical University</s1>
<s2>Izumo 693-8501</s2>
<s3>JPN</s3>
<sZ>2 aut.</sZ>
</fA14><fA15 i1="01"><s1>Department of Brain Sciences, Institute of Applied Biochemistry, Yagi Memorial Park</s1>
<s2>Mitake, Gifu 505-0116</s2>
<s3>JPN</s3>
<sZ>1 aut.</sZ>
</fA15><fA15 i1="02"><s1>Unit of Neuroendocrinology, Bat. 5, Parc Chateau, CNRS</s1>
<s2>91190 Gif sur Yvette</s2>
<s3>FRA</s3>
<sZ>2 aut.</sZ>
</fA15><fA15 i1="03"><s1>Laboratory of Biochemistry and Metabolism, Department of Basic Gerontology, National Institute of Longevity Sciences</s1>
<s2>Obu, Aichi 474-8622</s2>
<s3>JPN</s3>
<sZ>3 aut.</sZ>
</fA15><fA15 i1="04"><s1>Department of Molecular and Cellular Biochemistry, Loyola University of Chicago, Strich School of Medicine</s1>
<s2>Maywood, IL 60153</s2>
<s3>USA</s3>
<sZ>4 aut.</sZ>
</fA15><fA15 i1="05"><s1>Eve Topf and National Parkinson Foundation Neurodegenerative Diseases Centers, Department of Pharmacology, Rappaport Faculty of Medicine, Technion</s1>
<s2>Haifa 31096</s2>
<s3>ISR</s3>
<sZ>5 aut.</sZ>
</fA15><fA20><s1>593-598</s1>
</fA20><fA21><s1>2002</s1>
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</fA60><fA64 i1="01" i2="1"><s0>Neurotoxicology and teratology</s0>
</fA64><fA66 i1="01"><s0>USA</s0>
</fA66><fC01 i1="01" l="ENG"><s0>The discovery of 1-methyl-4-phenyl-1,2,2,6-tetrahydropyridine (MPTP) leads to the hypothesis that Parkinson's disease (PD) is may be initiated or precipitated by environmental or endogenous toxins by the mechanism similar to that of MPTP in genetically-predisposed individuals. Endogenous analogs of MPTP, such as β-carbolines (βCs) and tetrahydroisoquinolines, have been proposed as possible causative candidates causing PD and are bioactivated into potential neurotoxins by N-methylation enzyme(s). These N-methylated βCs and tetrahydroisoquinoline have been higher cerebrospinal levels in parkinsonian patients than age-matched controls. Thus, there is a hypotheses to influence the pathogenesis of PD, that is, the excess enzyme activity to activate neurotoxins, such as N-methyltransferase, might be higher in PDs. Indeed, simple βCs, via N-methylation steps, induced bradykinesia with the decreased dopamine contents in the striatum and midbrain in C57/BL mice. In younger (65 years old) PD patients, the excretion amount of N<sup>1</sup>
-methyl-nicotinamaide was significantly higher than that in younger controls. The protein amount of nicotinamide N-methyltransferase (NNMT) was also significantly higher in younger PD patients than that in younger controls. These findings described here would indicate that the excess N-methylation ability for azaheterocyclic amines, such as βCs, before the onset had been implicated in PD pathogenesis. On the other hand, the contribution of aberrant cytochrome P450 or aldehyde oxidase activity acting on the pyridine ring, that could act as detoxification routes of endogenous neurotoxins, would be small in the etiology of PD.</s0><fC02 i1="01" i2="X"><s0>002B17G</s0>
</fC02><fC03 i1="01" i2="X" l="FRE"><s0>Carboline dérivé</s0>
<s2>FR</s2>
<s5>01</s5>
</fC03><fC03 i1="01" i2="X" l="ENG"><s0>Carboline derivatives</s0>
<s2>FR</s2>
<s5>01</s5>
</fC03><fC03 i1="02" i2="X" l="FRE"><s0>Toxicité</s0>
<s5>04</s5>
</fC03><fC03 i1="02" i2="X" l="ENG"><s0>Toxicity</s0>
<s5>04</s5>
</fC03><fC03 i1="02" i2="X" l="SPA"><s0>Toxicidad</s0>
<s5>04</s5>
</fC03><fC03 i1="03" i2="X" l="FRE"><s0>Méthylation</s0>
<s5>07</s5>
</fC03><fC03 i1="03" i2="X" l="ENG"><s0>Methylation</s0>
<s5>07</s5>
</fC03><fC03 i1="03" i2="X" l="SPA"><s0>Metilación</s0>
<s5>07</s5>
</fC03><fC03 i1="04" i2="X" l="FRE"><s0>Parkinson maladie</s0>
<s5>10</s5>
</fC03><fC03 i1="04" i2="X" l="ENG"><s0>Parkinson disease</s0>
<s5>10</s5>
</fC03><fC03 i1="04" i2="X" l="SPA"><s0>Parkinson enfermedad</s0>
<s5>10</s5>
</fC03><fC03 i1="05" i2="X" l="FRE"><s0>Etiologie</s0>
<s5>11</s5>
</fC03><fC03 i1="05" i2="X" l="ENG"><s0>Etiology</s0>
<s5>11</s5>
</fC03><fC03 i1="05" i2="X" l="SPA"><s0>Etiología</s0>
<s5>11</s5>
</fC03><fC03 i1="06" i2="X" l="FRE"><s0>Pathogénie</s0>
<s5>12</s5>
</fC03><fC03 i1="06" i2="X" l="ENG"><s0>Pathogenesis</s0>
<s5>12</s5>
</fC03><fC03 i1="06" i2="X" l="SPA"><s0>Patogenia</s0>
<s5>12</s5>
</fC03><fC03 i1="07" i2="X" l="FRE"><s0>Homme</s0>
<s5>13</s5>
</fC03><fC03 i1="07" i2="X" l="ENG"><s0>Human</s0>
<s5>13</s5>
</fC03><fC03 i1="07" i2="X" l="SPA"><s0>Hombre</s0>
<s5>13</s5>
</fC03><fC07 i1="01" i2="X" l="FRE"><s0>Système nerveux pathologie</s0>
<s5>61</s5>
</fC07><fC07 i1="01" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>61</s5>
</fC07><fC07 i1="01" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>61</s5>
</fC07><fC07 i1="02" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0>
<s5>62</s5>
</fC07><fC07 i1="02" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>62</s5>
</fC07><fC07 i1="02" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>62</s5>
</fC07><fC07 i1="03" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>63</s5>
</fC07><fC07 i1="03" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>63</s5>
</fC07><fC07 i1="03" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>63</s5>
</fC07><fC07 i1="04" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0>
<s5>64</s5>
</fC07><fC07 i1="04" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>64</s5>
</fC07><fC07 i1="04" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>64</s5>
</fC07><fC07 i1="05" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>65</s5>
</fC07><fC07 i1="05" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>65</s5>
</fC07><fC07 i1="05" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>65</s5>
</fC07><fN21><s1>006</s1>
</fN21><fN82><s1>PSI</s1>
</fN82><pR><fA30 i1="01" i2="1" l="ENG"><s1>International Catecholamine Symposium</s1>
<s2>9</s2>
<s3>Kyoto JPN</s3>
<s4>2001-03-31</s4>
</fA30><fA30 i1="02" i2="1" l="ENG"><s1>International Joint Congresses on Progress in Alzheimer's and Parkinson's Disease</s1>
<s2>5</s2>
<s3>Kyoto JPN</s3>
<s4>2001-03-31</s4>
</fA30><server><NO>PASCAL 03-0018075 INIST</NO>
<ET>N-methylation underlying Parkinson's disease</ET>
<AU>MATSUBARA (Kazuo); AOYAMA (Koji); SUNO (Manabu); AWAYA (Toshio); NAOI (Makoto); PARVEZ (Hasan); MARUYAMA (Wakako); COLLINS (Michel A.); YOUDIM (Moussa B. H.)</AU>
<AF>Department of Hospital Pharmacy and Pharmacology, Asahikawa Medical College/Asahikawa 078-8510/Japon (1 aut., 3 aut., 4 aut.); Department of Internal Medicine III, Shimane Medical University/Izumo 693-8501/Japon (2 aut.); Department of Brain Sciences, Institute of Applied Biochemistry, Yagi Memorial Park/Mitake, Gifu 505-0116/Japon (1 aut.); Unit of Neuroendocrinology, Bat. 5, Parc Chateau, CNRS/91190 Gif sur Yvette/France (2 aut.); Laboratory of Biochemistry and Metabolism, Department of Basic Gerontology, National Institute of Longevity Sciences/Obu, Aichi 474-8622/Japon (3 aut.); Department of Molecular and Cellular Biochemistry, Loyola University of Chicago, Strich School of Medicine/Maywood, IL 60153/Etats-Unis (4 aut.); Eve Topf and National Parkinson Foundation Neurodegenerative Diseases Centers, Department of Pharmacology, Rappaport Faculty of Medicine, Technion/Haifa 31096/Israël (5 aut.)</AF>
<DT>Publication en série; Congrès; Niveau analytique</DT>
<SO>Neurotoxicology and teratology; ISSN 0892-0362; Coden NETEEC; Etats-Unis; Da. 2002; Vol. 24; No. 5; Pp. 593-598; Bibl. 32 ref.</SO>
<LA>Anglais</LA>
<EA>The discovery of 1-methyl-4-phenyl-1,2,2,6-tetrahydropyridine (MPTP) leads to the hypothesis that Parkinson's disease (PD) is may be initiated or precipitated by environmental or endogenous toxins by the mechanism similar to that of MPTP in genetically-predisposed individuals. Endogenous analogs of MPTP, such as β-carbolines (βCs) and tetrahydroisoquinolines, have been proposed as possible causative candidates causing PD and are bioactivated into potential neurotoxins by N-methylation enzyme(s). These N-methylated βCs and tetrahydroisoquinoline have been higher cerebrospinal levels in parkinsonian patients than age-matched controls. Thus, there is a hypotheses to influence the pathogenesis of PD, that is, the excess enzyme activity to activate neurotoxins, such as N-methyltransferase, might be higher in PDs. Indeed, simple βCs, via N-methylation steps, induced bradykinesia with the decreased dopamine contents in the striatum and midbrain in C57/BL mice. In younger (65 years old) PD patients, the excretion amount of N<sup>1</sup>
-methyl-nicotinamaide was significantly higher than that in younger controls. The protein amount of nicotinamide N-methyltransferase (NNMT) was also significantly higher in younger PD patients than that in younger controls. These findings described here would indicate that the excess N-methylation ability for azaheterocyclic amines, such as βCs, before the onset had been implicated in PD pathogenesis. On the other hand, the contribution of aberrant cytochrome P450 or aldehyde oxidase activity acting on the pyridine ring, that could act as detoxification routes of endogenous neurotoxins, would be small in the etiology of PD.</EA><CC>002B17G</CC>
<FD>Carboline dérivé; Toxicité; Méthylation; Parkinson maladie; Etiologie; Pathogénie; Homme</FD>
<FG>Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative</FG>
<ED>Carboline derivatives; Toxicity; Methylation; Parkinson disease; Etiology; Pathogenesis; Human</ED>
<EG>Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease</EG>
<SD>Toxicidad; Metilación; Parkinson enfermedad; Etiología; Patogenia; Hombre</SD>
<LO>INIST-18910.354000109244300040</LO>
<ID>03-0018075</ID>
</server>
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