Antiparkinsonian drugs and their neuroprotective effects.
In Parkinson's disease, while dopamine (DA) replacement therapy, such as with L-DOPA (levodopa), improves the symptoms, it does not inhibit the degeneration of DA neurons in the substantia nigra. Numerous studies have suggested that both endogenous and environmental neurotoxins and oxidative stress may participate in this disease, but the detailed mechanisms are still unclear. Recent genetic studies in familial Parkinson's disease and parkinsonism have shown several gene mutations. This new information regarding its pathogenesis offers novel prospects for effective strategies involving the neuroprotection of vulnerable DA neurons. This review summarizes current findings regarding the pathogenesis and antiparkinsonian drugs, and discusses their possibilities of targets to develop novel neuroprotective drugs.
Kitamura
Yoshihisa
Y
Department of Neurobiology, Kyoto Pharmaceutical University, Japan. yo-kita@mb.kyoto-phu.ac.jp
Kakimura
Jun-Ichi
J
Taniguchi
Takashi
T
D000978:Antiparkinson Agents / Q000494:pharmacology / Q000627:therapeutic use*; D017209:Apoptosis; D004298:Dopamine / Q000096:biosynthesis / Q000378:metabolism; D006801:Humans; D008025:Ligases / Q000502:physiology; D009419:Nerve Tissue Proteins / Q000502:physiology; D009474:Neurons / Q000473:pathology; D018696:Neuroprotective Agents / Q000494:pharmacology / Q000627:therapeutic use*; D010300:Parkinson Disease / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D011954:Receptors, Dopamine / Q000378:metabolism; D051843:Synucleins; D044767:Ubiquitin-Protein Ligases
D000978:Antiparkinson Agents; D009419:Nerve Tissue Proteins; D018696:Neuroprotective Agents; D011954:Receptors, Dopamine; D051843:Synucleins; D044767:Ubiquitin-Protein Ligases; C111567:parkin protein; D008025:Ligases; D004298:Dopamine