1、Need 2/3Hughes et al.JNNP;55:181-184Hughes et al.JNNP;55:181-184Hughes et al.JNNP;55:181-184Huse et al.Mov Disord 2005;20:1449-1454Kim et al.Mov Disord 2002;17:303-312Tofaris&Spillantini.Mov Disord 2005;20 Suppl 12:S37-44.Braak et al.Neurobiol Aging 2003;24:197-211Ubiquitin-dependentproteasomal prot
2、eolysisSystem failureSusceptibility Expression of UPS componentsAge-related UPS activityOxidative dopamine metabolismToxic processesOxidative stressMitochondrial dysfunctionToxinsGene mutations-synucleinParkinUCH L1LRRK2Protein accumulationCell dysfunctionLewy body formationCell deathmodified from M
3、cNaught&Olanow.Ann Neurol 2003;53:S73-86.Mandel et al.CNS Drugs 2003;17(10):729-762.more than 5000 research subjects no definite neuroprotective agentadapted from Jenner.Neurology 2002;58:S1-8.AAN Practice Parameter,1992;updated October 2005“In patients with PD who require the initiation of dopamine
4、rgic treatment,either levodopa or a dopamine agonist may be used.The choice depends on the relative impact of improving motor disability(better with levodopa)compared with the lessening of motor complications(better with dopamine agonists)for each individual patient with PD(level A,class I and class II evidence).”AAN Practice Parameter,1992;updated October 2005modified from Olanow et al.Neurology 2001;56(11 Suppl 5)S1-88)carbidopaselegilinetolcaponeentacaponeMcKeith et al.Neurology 2005;65:1863.
