Table 1.

Examples of rodent models used to study Parkinson's disease genes

Genetic modelDescriptionPD phenotypeReference
Motor deficitsDA neuron degenerationα-Synuclein pathology
α-Synuclein (PARK1, PARK4)Overexpression of WT α-synuclein using PDGF-β promoterYesSubtle defectsYesMasliah et al. (2000)
Expression of A53T mutant α-synuclein using mouse prion promoterYes (lethal)NoYesGiasson et al. (2002); Lee et al. (2002)
Expression of A30P mutant α-synuclein using Prp promoterYes (progressive)NoAtypicalGomez-Isla et al. (2003)
Lentivirus injection of WT or A30P (rat)NoYesYesLo Bianco et al. (2002)
Parkin (PARK2)Knock-outSubtleNoNoGoldberg et al. (2003); Itier et al. (2003)
Expression of mutant parkin-Q311X using dopamine transporter promoter in a bacterial artificial chromosomeYes (progressive)Yes (selective and progressive)AtypicalLu et al. (2009)
DJ-1 (PARK7)Knock-outYesSubtle defectsNoGoldberg et al. (2005); Chen et al. (2005)
PINK1 (PARK6)Knock-outYesSubtle defectsNoKitada et al. (2007)
Engrailed (En1 +/−)Knock-outYesYes (selective and progressive)NoLe Pen et al. (2008)
MitoPark (Tfam)Conditional knock-out, using Cre expressed in dopaminergic neurons (dopamine transporter promoter-Cre)Yes (progressive)Yes (selective and progressive)AtypicalEkstrand et al. (2007)
  • Advantages and disadvantages of different models are evaluated using three criteria: (1) motor deficits, (2) DA neuron degeneration, and (3) pathological changes in neurons. All are mouse models except where indicated.