Abstract
It has been over three decades since the introduction of L-dihydroxyphenylalanine or levodopa therapy for Parkinson's disease (PD). The early levodopa trials were driven by recognition of a profound cerebral dopamine deficiency 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 decarboxylase, replenishing central dopamine stores and potentially reversing the motor symptoms of PD.
MeSH terms
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Antiparkinson Agents / adverse effects
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Antiparkinson Agents / therapeutic use*
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Brain Tissue Transplantation
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Catechol O-Methyltransferase Inhibitors
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Cerebral Cortex / cytology
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Cerebral Cortex / embryology
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Cerebral Cortex / transplantation
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Clinical Trials as Topic
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Dopamine Agonists / adverse effects
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Dopamine Agonists / therapeutic use
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Drug Therapy, Combination
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Fetal Tissue Transplantation
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Globus Pallidus / surgery
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Humans
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Levodopa / adverse effects
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Levodopa / therapeutic use
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Neurons / transplantation
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Parkinson Disease / drug therapy*
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Parkinson Disease / surgery*
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Subthalamic Nucleus / surgery
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Thalamus / surgery
Substances
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Antiparkinson Agents
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Catechol O-Methyltransferase Inhibitors
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Dopamine Agonists
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Levodopa