Coenzyme Q10, Hyperhomocysteinemia and MTHFR C677T Polymorphism in Levodopa-treated Parkinson’s Disease Patients

作者: Gaetano Gorgone , Monica Currò , Nadia Ferlazzo , Giulia Parisi , Lucilla Parnetti

DOI: 10.1007/S12017-012-8174-1

关键词: EndocrinologyGene polymorphismHyperhomocysteinemiaOxidative stressGenotypeMethylenetetrahydrofolate reductaseInternal medicineMedicineCoenzyme Q10BiochemistryVitamin B12Homocysteine

摘要: There is evidence that increased homocysteine (Hcy) levels might accelerate dopaminergic cell death in Parkinson's disease (PD) through neurotoxic effects. Homocysteine neurotoxicity mainly relies on redox state alterations. The present work was aimed at investigating the relationships between plasma Hcy concentrations and percent content of oxidized versus total Coenzyme Q10 (%CoQ10) 60 PD patients 82 healthy subjects. Both groups were screened for Hcy, vitamin B12, folate, %CoQ10 C677T methylenetetrahydrofolate reductase (MTHFR) gene polymorphism. MTHFR TT677 mutated genotype found more frequently than controls (p = 0.01). In a multivariate analysis, associated with case/control category < 0.0001), 0.0001) their interaction term 0.0015), even after adjusting age, sex, folate B12. Patients carrying exhibited highest values 0.0001). Structural equation modelling evidenced levodopa daily dose independently directly correlated 0.0001, p 0.003, respectively), which, turn, showed significant correlation patients. Our results suggest act as mediator systemic oxidative stress occurring PD, determination be regarded predictor toxic

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