28 Citations (Scopus)

Abstract

Genetic C677T and A1298C polymorphisms in 5,10-methylenetetrahydrofolate reductase (MTHFR) and levodopa therapy in Parkinson's disease (PD) may increase homocysteine (Hcy) level. We examined whether connecting both polymorphisms influences the effect of levodopa on Hcy. MTHFR genotypes and Hcy, vitamin B12, and folate levels were determined in 48 levodopa-treated PD patients (PD-L), 28 non-treated PD patients (PD-N) and 110 controls. Hcy was remarkably higher in PD-L than in PD-N and controls (p <0.001); similarly, the differences were seen in different age subgroups and in both genders. Furthermore, Hcy differences between PD-L and PD-N were evident in 677C/T, T/T, C/T + A/A, T/T + A/A (all p <0.05), and 1298A/A (p <0.001), but not in others such as 677C/C, and C/C + A/A. Hcy in PD-N and controls was comparable for all genotypes. In PD-L, Hcy was the highest in 677T/T, then in C/T, and in C/C with a significant difference from T/T (p = 0.014), but was not different among A1298C genotypes. Likewise, Hcy was the highest in 677T/T + 1298A/A, intermediate in C/T + A/A, and the lowest in C/C + A/A. In PD-N, Hcy was similar among all genotypes. In conclusion, Hcy elevation may be caused by levodopa administration, and further promoted by 677C/T and T/T, but not by A1298C genotypes. The promoting elevation in 1298A/A is attributed to combining the 677T allele. Neither C677T nor A1298C genotypes contribute to elevating Hcy in PD-N.

Original languageEnglish
Pages (from-to)64-68
Number of pages5
JournalJournal of the Neurological Sciences
Volume287
Issue number1-2
DOIs
Publication statusPublished - Dec 15 2009

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Methylenetetrahydrofolate Reductase (NADPH2)
Levodopa
Homocysteine
Parkinson Disease
Genotype
Vitamin B 12
Folic Acid

Keywords

  • A1298C
  • C677T
  • Homocysteine
  • MTHFR
  • Parkinson's disease
  • Polymorphism

ASJC Scopus subject areas

  • Clinical Neurology
  • Neurology

Cite this

Methylenetetrahydrofolate reductase polymorphisms and plasma homocysteine in levodopa-treated and non-treated Parkinson's disease patients. / Yuan, Rey Yue; Sheu, Jau Jiuan; Yu, Jia Ming; Hu, Chaur Jong; Tseng, Ing Jy; Ho, Chun Sum; Yeh, Ching-Ying; Hung, Ya Lin; Chiang, Tsuey Ru.

In: Journal of the Neurological Sciences, Vol. 287, No. 1-2, 15.12.2009, p. 64-68.

Research output: Contribution to journalArticle

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abstract = "Genetic C677T and A1298C polymorphisms in 5,10-methylenetetrahydrofolate reductase (MTHFR) and levodopa therapy in Parkinson's disease (PD) may increase homocysteine (Hcy) level. We examined whether connecting both polymorphisms influences the effect of levodopa on Hcy. MTHFR genotypes and Hcy, vitamin B12, and folate levels were determined in 48 levodopa-treated PD patients (PD-L), 28 non-treated PD patients (PD-N) and 110 controls. Hcy was remarkably higher in PD-L than in PD-N and controls (p <0.001); similarly, the differences were seen in different age subgroups and in both genders. Furthermore, Hcy differences between PD-L and PD-N were evident in 677C/T, T/T, C/T + A/A, T/T + A/A (all p <0.05), and 1298A/A (p <0.001), but not in others such as 677C/C, and C/C + A/A. Hcy in PD-N and controls was comparable for all genotypes. In PD-L, Hcy was the highest in 677T/T, then in C/T, and in C/C with a significant difference from T/T (p = 0.014), but was not different among A1298C genotypes. Likewise, Hcy was the highest in 677T/T + 1298A/A, intermediate in C/T + A/A, and the lowest in C/C + A/A. In PD-N, Hcy was similar among all genotypes. In conclusion, Hcy elevation may be caused by levodopa administration, and further promoted by 677C/T and T/T, but not by A1298C genotypes. The promoting elevation in 1298A/A is attributed to combining the 677T allele. Neither C677T nor A1298C genotypes contribute to elevating Hcy in PD-N.",
keywords = "A1298C, C677T, Homocysteine, MTHFR, Parkinson's disease, Polymorphism",
author = "Yuan, {Rey Yue} and Sheu, {Jau Jiuan} and Yu, {Jia Ming} and Hu, {Chaur Jong} and Tseng, {Ing Jy} and Ho, {Chun Sum} and Ching-Ying Yeh and Hung, {Ya Lin} and Chiang, {Tsuey Ru}",
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T1 - Methylenetetrahydrofolate reductase polymorphisms and plasma homocysteine in levodopa-treated and non-treated Parkinson's disease patients

AU - Yuan, Rey Yue

AU - Sheu, Jau Jiuan

AU - Yu, Jia Ming

AU - Hu, Chaur Jong

AU - Tseng, Ing Jy

AU - Ho, Chun Sum

AU - Yeh, Ching-Ying

AU - Hung, Ya Lin

AU - Chiang, Tsuey Ru

PY - 2009/12/15

Y1 - 2009/12/15

N2 - Genetic C677T and A1298C polymorphisms in 5,10-methylenetetrahydrofolate reductase (MTHFR) and levodopa therapy in Parkinson's disease (PD) may increase homocysteine (Hcy) level. We examined whether connecting both polymorphisms influences the effect of levodopa on Hcy. MTHFR genotypes and Hcy, vitamin B12, and folate levels were determined in 48 levodopa-treated PD patients (PD-L), 28 non-treated PD patients (PD-N) and 110 controls. Hcy was remarkably higher in PD-L than in PD-N and controls (p <0.001); similarly, the differences were seen in different age subgroups and in both genders. Furthermore, Hcy differences between PD-L and PD-N were evident in 677C/T, T/T, C/T + A/A, T/T + A/A (all p <0.05), and 1298A/A (p <0.001), but not in others such as 677C/C, and C/C + A/A. Hcy in PD-N and controls was comparable for all genotypes. In PD-L, Hcy was the highest in 677T/T, then in C/T, and in C/C with a significant difference from T/T (p = 0.014), but was not different among A1298C genotypes. Likewise, Hcy was the highest in 677T/T + 1298A/A, intermediate in C/T + A/A, and the lowest in C/C + A/A. In PD-N, Hcy was similar among all genotypes. In conclusion, Hcy elevation may be caused by levodopa administration, and further promoted by 677C/T and T/T, but not by A1298C genotypes. The promoting elevation in 1298A/A is attributed to combining the 677T allele. Neither C677T nor A1298C genotypes contribute to elevating Hcy in PD-N.

AB - Genetic C677T and A1298C polymorphisms in 5,10-methylenetetrahydrofolate reductase (MTHFR) and levodopa therapy in Parkinson's disease (PD) may increase homocysteine (Hcy) level. We examined whether connecting both polymorphisms influences the effect of levodopa on Hcy. MTHFR genotypes and Hcy, vitamin B12, and folate levels were determined in 48 levodopa-treated PD patients (PD-L), 28 non-treated PD patients (PD-N) and 110 controls. Hcy was remarkably higher in PD-L than in PD-N and controls (p <0.001); similarly, the differences were seen in different age subgroups and in both genders. Furthermore, Hcy differences between PD-L and PD-N were evident in 677C/T, T/T, C/T + A/A, T/T + A/A (all p <0.05), and 1298A/A (p <0.001), but not in others such as 677C/C, and C/C + A/A. Hcy in PD-N and controls was comparable for all genotypes. In PD-L, Hcy was the highest in 677T/T, then in C/T, and in C/C with a significant difference from T/T (p = 0.014), but was not different among A1298C genotypes. Likewise, Hcy was the highest in 677T/T + 1298A/A, intermediate in C/T + A/A, and the lowest in C/C + A/A. In PD-N, Hcy was similar among all genotypes. In conclusion, Hcy elevation may be caused by levodopa administration, and further promoted by 677C/T and T/T, but not by A1298C genotypes. The promoting elevation in 1298A/A is attributed to combining the 677T allele. Neither C677T nor A1298C genotypes contribute to elevating Hcy in PD-N.

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