Homocysteine and levodopa: should Parkinson disease patients receive preventative therapy?

Neurology. 2004 Sep 14;63(5):886-91. doi: 10.1212/01.wnl.0000137886.74175.5a.

Abstract

Epidemiologic evidence has linked elevation of serum homocysteine to an increased risk of coronary artery disease, stroke, and dementia. An increase in homocysteine levels in Parkinson disease (PD) recently has been discovered. Although B vitamin status and genetic factors are important modifying influences determining the degree of this elevation, the main cause appears to be therapy with L-dopa. It has been suggested that breakdown of L-dopa by catechol-O-methyltransferase results in increased homocysteine formation. Therefore, there are reasons to suggest that management of PD may render patients at increased risk of stroke, heart disease, dementia, and even accelerated nigral degeneration. At present, no controlled prospective studies have evaluated this phenomenon, although they are ongoing.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Antiparkinson Agents / adverse effects*
  • Antiparkinson Agents / therapeutic use
  • Arteriosclerosis / etiology
  • Arteriosclerosis / prevention & control*
  • Catechol O-Methyltransferase / metabolism
  • Dementia / etiology
  • Dementia / prevention & control
  • Disease Progression
  • Disease Susceptibility
  • Homocysteine / biosynthesis*
  • Homocysteine / blood
  • Humans
  • Hyperhomocysteinemia / chemically induced*
  • Hyperhomocysteinemia / complications
  • Hyperhomocysteinemia / physiopathology
  • Inflammation
  • Levodopa / adverse effects*
  • Levodopa / pharmacokinetics
  • Levodopa / therapeutic use
  • Models, Biological
  • Multicenter Studies as Topic
  • Oxidative Stress
  • Parkinson Disease / drug therapy*
  • Parkinson Disease / metabolism
  • Randomized Controlled Trials as Topic
  • Substantia Nigra / drug effects

Substances

  • Antiparkinson Agents
  • Homocysteine
  • Levodopa
  • Catechol O-Methyltransferase