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Methylenetetrahydrofolate reductase polymorphisms and plasma homocysteine in levodopa-treated and non-treated Parkinson's disease patients.
J Neurol Sci. 2009 Dec 15; 287(1-2):64-8.JN

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 B(12), 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.

Links

Publisher Full Text (DOI)

Authors+Show Affiliations

Yuan RY
Department of Neurology, Taipei Medical University Hospital, Taipei, Taiwan.
Sheu JJ
No affiliation info available
Yu JM
No affiliation info available
Hu CJ
No affiliation info available
Tseng IJ
No affiliation info available
Ho CS
No affiliation info available
Yeh CY
No affiliation info available
Hung YL
No affiliation info available
Chiang TR
No affiliation info available

MeSH

Age DistributionAgedAged, 80 and overAmino Acid SubstitutionAntiparkinson AgentsBase SequenceBiomarkersDNA Mutational AnalysisFemaleGene FrequencyGenetic MarkersGenetic Predisposition to DiseaseGenetic TestingGenotypeHomocysteineHumansLevodopaMaleMethylenetetrahydrofolate Dehydrogenase (NAD+)Parkinson DiseasePolymorphism, GeneticSex Distribution

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19786283

Citation

Yuan, Rey-Yue, et al. "Methylenetetrahydrofolate Reductase Polymorphisms and Plasma Homocysteine in Levodopa-treated and Non-treated Parkinson's Disease Patients." Journal of the Neurological Sciences, vol. 287, no. 1-2, 2009, pp. 64-8.
Yuan RY, Sheu JJ, Yu JM, et al. Methylenetetrahydrofolate reductase polymorphisms and plasma homocysteine in levodopa-treated and non-treated Parkinson's disease patients. J Neurol Sci. 2009;287(1-2):64-8.
Yuan, R. Y., Sheu, J. J., Yu, J. M., Hu, C. J., Tseng, I. J., Ho, C. S., Yeh, C. Y., Hung, Y. L., & Chiang, T. R. (2009). Methylenetetrahydrofolate reductase polymorphisms and plasma homocysteine in levodopa-treated and non-treated Parkinson's disease patients. Journal of the Neurological Sciences, 287(1-2), 64-8. https://doi.org/10.1016/j.jns.2009.09.007
Yuan RY, et al. Methylenetetrahydrofolate Reductase Polymorphisms and Plasma Homocysteine in Levodopa-treated and Non-treated Parkinson's Disease Patients. J Neurol Sci. 2009 Dec 15;287(1-2):64-8. PubMed PMID: 19786283.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR 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, Y1 - 2009/09/27/ PY - 2009/05/05/received PY - 2009/09/03/revised PY - 2009/09/08/accepted PY - 2009/9/30/entrez PY - 2009/9/30/pubmed PY - 2010/2/13/medline SP - 64 EP - 8 JF - Journal of the neurological sciences JO - J Neurol Sci VL - 287 IS - 1-2 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 B(12), 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. SN - 1878-5883 UR - https://www.unboundmedicine.com/medline/citation/19786283/Methylenetetrahydrofolate_reductase_polymorphisms_and_plasma_homocysteine_in_levodopa_treated_and_non_treated_Parkinson's_disease_patients_ DB - PRIME DP - Unbound Medicine ER -