It has been over three decades since the introduction of L-dihydroxyphenyla
lanine or levodopa therapy for Parkinson's disease (PD). The early levodopa
trials were driven by recognition of a profound cerebral dopamine deficien
cy state in this disorder. Whereas dopamine fails to cross the blood brain
barrier and hence is ineffective as therapy, the amino acid precursor, dopa
, is transported across this barrier and provides a substrate for dopamine
synthesis. Levodopa is converted to dopamine within the brain by dopa decar
boxylase, replenishing central dopamine stores and potentially reversing th
e motor symptoms of PD.