Abstract
Several separate gene mutations have now been identified in familial Parkinson's disease and important environmental influences modulating risk for the idiopathic form of the disease have also been recognised. These insights have provided important clues in the development of disease modifying therapies. Some compounds have already been shown to potentially delay disease progression in early clinical trials. The most important challenge, particularly for those drugs that might have a symptomatic effect, is defining appropriate markers that will confirm a neuroprotective effect.
MeSH terms
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Antiparkinson Agents / pharmacology*
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Biomarkers / analysis
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Environmental Exposure / adverse effects
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Free Radical Scavengers / pharmacology
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Free Radical Scavengers / therapeutic use
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Genetic Predisposition to Disease / genetics
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Humans
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Nerve Tissue Proteins / deficiency
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Nerve Tissue Proteins / genetics
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Neuroprotective Agents / pharmacology
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Neuroprotective Agents / therapeutic use
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Oxidative Stress / physiology
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Parkinson Disease / drug therapy*
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Parkinson Disease / genetics
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Parkinson Disease / physiopathology
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Synucleins
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Treatment Outcome
Substances
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Antiparkinson Agents
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Biomarkers
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Free Radical Scavengers
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Nerve Tissue Proteins
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Neuroprotective Agents
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Synucleins