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
|