ParkinsonFranceV1, PascalFrancis, Checkpoint, bibRecord, 000F15

N-methylation underlying Parkinson's disease

Identifieur interne : 000F15 ( PascalFrancis/Checkpoint ); précédent : 000F14; suivant : 000F16

N-methylation underlying Parkinson's disease

Auteurs : Kazuo Matsubara [Japon] ; Koji Aoyama [Japon] ; Manabu Suno [Japon] ; Toshio Awaya [Japon]

Source :

Neurotoxicology and teratology [ 0892-0362 ] ; 2002.

RBID : Pascal:03-0018075

Descripteurs français

Pascal (Inist)
- Carboline dérivé, Toxicité, Méthylation, Parkinson maladie, Etiologie, Pathogénie, Homme.
Wicri :
- topic : Homme.

English descriptors

KwdEn :
- Carboline derivatives, Etiology, Human, Methylation, Parkinson disease, Pathogenesis, Toxicity.

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.

Affiliations:

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Le document en format XML

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<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>
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-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>
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<name sortKey="Awaya, Toshio" sort="Awaya, Toshio" uniqKey="Awaya T" first="Toshio" last="Awaya">Toshio Awaya</name>
<name sortKey="Suno, Manabu" sort="Suno, Manabu" uniqKey="Suno M" first="Manabu" last="Suno">Manabu Suno</name>
</country>
</tree>
</affiliations>
</record>

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EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonFranceV1/Data/PascalFrancis/Checkpoint

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000F15 | SxmlIndent | more

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Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Wicri/Sante
   |area=    ParkinsonFranceV1
   |flux=    PascalFrancis
   |étape=   Checkpoint
   |type=    RBID
   |clé=     Pascal:03-0018075
   |texte=   N-methylation underlying Parkinson's disease
}}

This area was generated with Dilib version V0.6.29.
Data generation: Wed May 17 19:46:39 2017. Site generation: Mon Mar 4 15:48:15 2024

	La maladie de Parkinson en France (serveur d'exploration)
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

La maladie de Parkinson en France (serveur d'exploration)

N-methylation underlying Parkinson's disease

N-methylation underlying Parkinson's disease

Source :

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Abstract

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