Monoamine oxidase B rs1799836 G allele polymorphism is a risk factor for early development of levodopa-induced dyskinesia in Parkinson's disease.

Dopamine metabolism genes Dyskinesia MAO-B polymorphism Parkinson's disease

Journal

eNeurologicalSci
ISSN: 2405-6502
Titre abrégé: eNeurologicalSci
Pays: Netherlands
ID NLM: 101667077

Informations de publication

Date de publication:
Jun 2020
Historique:
received: 12 02 2019
revised: 31 03 2020
accepted: 02 04 2020
entrez: 30 4 2020
pubmed: 30 4 2020
medline: 30 4 2020
Statut: epublish

Résumé

Dopamine replacement therapy is an established treatment for motor symptoms of Parkinson's disease, but its long-term use is often limited by the eventual development of motor complications, including levodopa-induced dyskinesia. Genetic background, particularly polymorphisms of dopamine metabolism genes, may affect the occurrence of dyskinesia in Parkinson's disease patients. We investigated polymorphisms of dopamine metabolism genes, including catechol- Monoamine oxidase B rs1799836 was the only polymorphism correlated with risk of dyskinesia. Patients with an AG or GG genotype were more likely to have dyskinesia than those with an AA genotype (adjusted hazard ratio, 3.41; 95% confidence interval, 1.28-9.10). Also, Kaplan-Meier curves demonstrated that patients with an AG or GG genotype developed dyskinesia earlier than those with an AA genotype (log-rank test, In Parkinson's disease patients, the monoamine oxidase B rs1799836 G allele is associated with a greater likelihood of developing dyskinesia than the A allele, possibly due to its association with lower monoamine oxidase B activity in the brain. Thus, detection of monoamine oxidase B polymorphisms may be useful for determining the optimal dosing of antiparkinson medications.

Sections du résumé

BACKGROUND BACKGROUND
Dopamine replacement therapy is an established treatment for motor symptoms of Parkinson's disease, but its long-term use is often limited by the eventual development of motor complications, including levodopa-induced dyskinesia. Genetic background, particularly polymorphisms of dopamine metabolism genes, may affect the occurrence of dyskinesia in Parkinson's disease patients.
METHODS METHODS
We investigated polymorphisms of dopamine metabolism genes, including catechol-
RESULTS RESULTS
Monoamine oxidase B rs1799836 was the only polymorphism correlated with risk of dyskinesia. Patients with an AG or GG genotype were more likely to have dyskinesia than those with an AA genotype (adjusted hazard ratio, 3.41; 95% confidence interval, 1.28-9.10). Also, Kaplan-Meier curves demonstrated that patients with an AG or GG genotype developed dyskinesia earlier than those with an AA genotype (log-rank test,
CONCLUSIONS CONCLUSIONS
In Parkinson's disease patients, the monoamine oxidase B rs1799836 G allele is associated with a greater likelihood of developing dyskinesia than the A allele, possibly due to its association with lower monoamine oxidase B activity in the brain. Thus, detection of monoamine oxidase B polymorphisms may be useful for determining the optimal dosing of antiparkinson medications.

Identifiants

pubmed: 32346620
doi: 10.1016/j.ensci.2020.100239
pii: S2405-6502(20)30018-6
pii: 100239
pmc: PMC7183157
doi:

Types de publication

Journal Article

Langues

eng

Pagination

100239

Informations de copyright

© 2020 The Authors.

Déclaration de conflit d'intérêts

None.

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Auteurs

Shoko Kakinuma (S)

Department of Molecular Diagnosis, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba-shi, Chiba 260-8670, Japan.

Minako Beppu (M)

Department of Molecular Diagnosis, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba-shi, Chiba 260-8670, Japan.

Setsu Sawai (S)

Department of Neurology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba-shi, Chiba 260-8670, Japan.

Akitoshi Nakayama (A)

Department of Molecular Diagnosis, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba-shi, Chiba 260-8670, Japan.

Shigeki Hirano (S)

Department of Neurology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba-shi, Chiba 260-8670, Japan.

Yoshitaka Yamanaka (Y)

Department of Neurology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba-shi, Chiba 260-8670, Japan.

Tatsuya Yamamoto (T)

Department of Neurology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba-shi, Chiba 260-8670, Japan.

Chigusa Masafumi (C)

Department of Neurology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba-shi, Chiba 260-8670, Japan.

Xiamuxiya Aisihaer (X)

Department of Molecular Diagnosis, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba-shi, Chiba 260-8670, Japan.

Alimasi Aersilan (A)

Department of Molecular Diagnosis, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba-shi, Chiba 260-8670, Japan.

Yue Gao (Y)

Department of Molecular Diagnosis, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba-shi, Chiba 260-8670, Japan.

Kenichi Sato (K)

Department of Medical Technology and Sciences, International University of Health and Welfare, 2-4-16 Momochihama Sawara-ku, Fukuoka City, Fukuoka 814-0001, Japan.

Itoga Sakae (I)

Division of Laboratory Medicine, Chiba University Hospital, 1-8-1 Inohana, Chuo-ku, Chiba-shi, Chiba 260-8670, Japan.

Takayuki Ishige (T)

Division of Laboratory Medicine, Chiba University Hospital, 1-8-1 Inohana, Chuo-ku, Chiba-shi, Chiba 260-8670, Japan.

Motoi Nishimura (M)

Division of Laboratory Medicine, Chiba University Hospital, 1-8-1 Inohana, Chuo-ku, Chiba-shi, Chiba 260-8670, Japan.

Kazuyuki Matsushita (K)

Division of Laboratory Medicine, Chiba University Hospital, 1-8-1 Inohana, Chuo-ku, Chiba-shi, Chiba 260-8670, Japan.

Mamoru Satoh (M)

Clinical Proteomics Research Center, Chiba University Hospital, 1-8-1 Inohana, Chuo-ku, Chiba-shi, Chiba 260-8670, Japan.

Fumio Nomura (F)

Clinical Proteomics Research Center, Chiba University Hospital, 1-8-1 Inohana, Chuo-ku, Chiba-shi, Chiba 260-8670, Japan.

Satoshi Kuwabara (S)

Department of Neurology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba-shi, Chiba 260-8670, Japan.

Tomoaki Tanaka (T)

Department of Molecular Diagnosis, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba-shi, Chiba 260-8670, Japan.

Classifications MeSH