SNCA polymorphisms, smoking, and sporadic Parkinson's disease in Japanese

Yoshihiro Miyake, Keiko Tanaka, Wakaba Fukushima, Chikako Kiyohara, Satoshi Sasaki, Yoshio Tsuboi, Tatsuo Yamada, Tomoko Oeda, Hiroyuki Shimada, Nobutoshi Kawamura, Nobutaka Sakae, Hidenao Fukuyama, Yoshio Hirota, Masaki Nagai

研究成果: ジャーナルへの寄稿記事

20 引用 (Scopus)

抄録

Several case-control studies and genome-wide association studies have examined the relationships between single nucleotide polymorphisms (SNPs) in the SNCA gene and Parkinson's disease (PD), and have provided inconsistent results. We investigated the relationships between SNPs rs356229, rs356219, rs356220, rs7684318, and rs2736990 and the risk of sporadic PD in Japan using data from a multicenter hospital-based case-control study. Included were 229 cases within 6 years of onset of PD as defined according to the UK PD Society Brain Bank clinical diagnostic criteria. Controls were 357 inpatients and outpatients without neurodegenerative disease. Adjustment was made for sex, age, region of residence, and smoking. Based on the recessive model, compared with subjects with the CC or CT genotype of SNP rs356220, those with the TT genotype had a significantly increased risk of sporadic PD: the adjusted OR was 1.42 (95% CI: 1.002-2.02). In the additive model, SNP rs2736990 was significantly related to the risk of sporadic PD: the adjusted OR was 1.30 (95% CI: 1.002-1.68). There were no significant relationships between SNP rs356229, rs356219, or rs7684318 and the risk of sporadic PD in any genetic model. The additive interactions between SNPs rs356219 and rs356220 and smoking with respect to sporadic PD were significant although the multiplicative interactions were not significant. This study suggests that SNCA SNPs rs356220 and rs2736990 are significantly associated with the risk of sporadic PD in Japanese. We also present new evidence for biological interactions between SNPs rs356219 and rs356220 and smoking that affect sporadic PD.

元の言語英語
ページ(範囲)557-561
ページ数5
ジャーナルParkinsonism and Related Disorders
18
発行部数5
DOI
出版物ステータス出版済み - 6 1 2012

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Parkinson Disease
Smoking
Single Nucleotide Polymorphism
Case-Control Studies
Genotype
Social Adjustment
Genome-Wide Association Study
Genetic Models
Neurodegenerative Diseases
Inpatients
Japan
Outpatients
Brain
Genes

All Science Journal Classification (ASJC) codes

  • Neurology
  • Geriatrics and Gerontology
  • Clinical Neurology

これを引用

SNCA polymorphisms, smoking, and sporadic Parkinson's disease in Japanese. / Miyake, Yoshihiro; Tanaka, Keiko; Fukushima, Wakaba; Kiyohara, Chikako; Sasaki, Satoshi; Tsuboi, Yoshio; Yamada, Tatsuo; Oeda, Tomoko; Shimada, Hiroyuki; Kawamura, Nobutoshi; Sakae, Nobutaka; Fukuyama, Hidenao; Hirota, Yoshio; Nagai, Masaki.

:: Parkinsonism and Related Disorders, 巻 18, 番号 5, 01.06.2012, p. 557-561.

研究成果: ジャーナルへの寄稿記事

Miyake, Y, Tanaka, K, Fukushima, W, Kiyohara, C, Sasaki, S, Tsuboi, Y, Yamada, T, Oeda, T, Shimada, H, Kawamura, N, Sakae, N, Fukuyama, H, Hirota, Y & Nagai, M 2012, 'SNCA polymorphisms, smoking, and sporadic Parkinson's disease in Japanese', Parkinsonism and Related Disorders, 巻. 18, 番号 5, pp. 557-561. https://doi.org/10.1016/j.parkreldis.2012.02.016
Miyake, Yoshihiro ; Tanaka, Keiko ; Fukushima, Wakaba ; Kiyohara, Chikako ; Sasaki, Satoshi ; Tsuboi, Yoshio ; Yamada, Tatsuo ; Oeda, Tomoko ; Shimada, Hiroyuki ; Kawamura, Nobutoshi ; Sakae, Nobutaka ; Fukuyama, Hidenao ; Hirota, Yoshio ; Nagai, Masaki. / SNCA polymorphisms, smoking, and sporadic Parkinson's disease in Japanese. :: Parkinsonism and Related Disorders. 2012 ; 巻 18, 番号 5. pp. 557-561.
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abstract = "Several case-control studies and genome-wide association studies have examined the relationships between single nucleotide polymorphisms (SNPs) in the SNCA gene and Parkinson's disease (PD), and have provided inconsistent results. We investigated the relationships between SNPs rs356229, rs356219, rs356220, rs7684318, and rs2736990 and the risk of sporadic PD in Japan using data from a multicenter hospital-based case-control study. Included were 229 cases within 6 years of onset of PD as defined according to the UK PD Society Brain Bank clinical diagnostic criteria. Controls were 357 inpatients and outpatients without neurodegenerative disease. Adjustment was made for sex, age, region of residence, and smoking. Based on the recessive model, compared with subjects with the CC or CT genotype of SNP rs356220, those with the TT genotype had a significantly increased risk of sporadic PD: the adjusted OR was 1.42 (95{\%} CI: 1.002-2.02). In the additive model, SNP rs2736990 was significantly related to the risk of sporadic PD: the adjusted OR was 1.30 (95{\%} CI: 1.002-1.68). There were no significant relationships between SNP rs356229, rs356219, or rs7684318 and the risk of sporadic PD in any genetic model. The additive interactions between SNPs rs356219 and rs356220 and smoking with respect to sporadic PD were significant although the multiplicative interactions were not significant. This study suggests that SNCA SNPs rs356220 and rs2736990 are significantly associated with the risk of sporadic PD in Japanese. We also present new evidence for biological interactions between SNPs rs356219 and rs356220 and smoking that affect sporadic PD.",
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T1 - SNCA polymorphisms, smoking, and sporadic Parkinson's disease in Japanese

AU - Miyake, Yoshihiro

AU - Tanaka, Keiko

AU - Fukushima, Wakaba

AU - Kiyohara, Chikako

AU - Sasaki, Satoshi

AU - Tsuboi, Yoshio

AU - Yamada, Tatsuo

AU - Oeda, Tomoko

AU - Shimada, Hiroyuki

AU - Kawamura, Nobutoshi

AU - Sakae, Nobutaka

AU - Fukuyama, Hidenao

AU - Hirota, Yoshio

AU - Nagai, Masaki

PY - 2012/6/1

Y1 - 2012/6/1

N2 - Several case-control studies and genome-wide association studies have examined the relationships between single nucleotide polymorphisms (SNPs) in the SNCA gene and Parkinson's disease (PD), and have provided inconsistent results. We investigated the relationships between SNPs rs356229, rs356219, rs356220, rs7684318, and rs2736990 and the risk of sporadic PD in Japan using data from a multicenter hospital-based case-control study. Included were 229 cases within 6 years of onset of PD as defined according to the UK PD Society Brain Bank clinical diagnostic criteria. Controls were 357 inpatients and outpatients without neurodegenerative disease. Adjustment was made for sex, age, region of residence, and smoking. Based on the recessive model, compared with subjects with the CC or CT genotype of SNP rs356220, those with the TT genotype had a significantly increased risk of sporadic PD: the adjusted OR was 1.42 (95% CI: 1.002-2.02). In the additive model, SNP rs2736990 was significantly related to the risk of sporadic PD: the adjusted OR was 1.30 (95% CI: 1.002-1.68). There were no significant relationships between SNP rs356229, rs356219, or rs7684318 and the risk of sporadic PD in any genetic model. The additive interactions between SNPs rs356219 and rs356220 and smoking with respect to sporadic PD were significant although the multiplicative interactions were not significant. This study suggests that SNCA SNPs rs356220 and rs2736990 are significantly associated with the risk of sporadic PD in Japanese. We also present new evidence for biological interactions between SNPs rs356219 and rs356220 and smoking that affect sporadic PD.

AB - Several case-control studies and genome-wide association studies have examined the relationships between single nucleotide polymorphisms (SNPs) in the SNCA gene and Parkinson's disease (PD), and have provided inconsistent results. We investigated the relationships between SNPs rs356229, rs356219, rs356220, rs7684318, and rs2736990 and the risk of sporadic PD in Japan using data from a multicenter hospital-based case-control study. Included were 229 cases within 6 years of onset of PD as defined according to the UK PD Society Brain Bank clinical diagnostic criteria. Controls were 357 inpatients and outpatients without neurodegenerative disease. Adjustment was made for sex, age, region of residence, and smoking. Based on the recessive model, compared with subjects with the CC or CT genotype of SNP rs356220, those with the TT genotype had a significantly increased risk of sporadic PD: the adjusted OR was 1.42 (95% CI: 1.002-2.02). In the additive model, SNP rs2736990 was significantly related to the risk of sporadic PD: the adjusted OR was 1.30 (95% CI: 1.002-1.68). There were no significant relationships between SNP rs356229, rs356219, or rs7684318 and the risk of sporadic PD in any genetic model. The additive interactions between SNPs rs356219 and rs356220 and smoking with respect to sporadic PD were significant although the multiplicative interactions were not significant. This study suggests that SNCA SNPs rs356220 and rs2736990 are significantly associated with the risk of sporadic PD in Japanese. We also present new evidence for biological interactions between SNPs rs356219 and rs356220 and smoking that affect sporadic PD.

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