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  Česky / Czech version Čes. a slov. Neurol. Neurochir., 69/102, 2006, No. 3, p. 183–188.
 
Homocysteine, Levodopa and Parkinson’s Disease 
Valkovič P.1,2, Blažíček P.3, Benetin J.1, Kukumberg P.1 

1II. neurologická klinika LF UK, Bratislava 2Neurologische Klinik, Ludwig-Maximilians-Universität München 3Oddelenie klinických laboratórií, Nemocnica ministerstva obrany, Bratislava
 


Summary:

       Hyperhomocysteinemia is an independent risk factor at atherothrombotic vascular diseases, cognitive impairment, and dementia. Patients with Parkinson’s disease (PD) have a consistent increase in their plasma homocysteine (HCY) levels. This is caused mainly by a long-term treatment with levodopa, frequently on the background of the latent B-vitamin deficiency. Considering the fact that vascular morbidity and cognitive impairment seriously worsen the prognosis and course of PD, the increased HCY should be monitored meaningfully and treated adequately. Some recent smaller studies have indicated possible treatment approaches such as supplementation of B-vitamins (in particular folate and vitamin B12) and inhibition of the enzyme catechol-O-methyl-transferase (with entacapone). However, these promising findings must be confirmed now in controlled prospective trials.

        Key words: homocysteine, levodopa, Parkinson’s disease, B-vitamins, therapy
       

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