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Mouse

General Transgenic Models

Gene	Promoter/Background	Phenotype	Availability	Reference
Human α-synuclein: WT	PGDF-βC57BL/6 × DBA/2	α-syn inclusions (cytoplasmic and intranuclear) in neocortex, hippocampus, and substantia nigra. Loss of dopaminergic terminals and motor impairment.		Masliah et al. Science 2000; 287(5456):1265-9
Human α-synuclein: A53T	Murine PrpC57Bl/C3H	α-syn fibrillar inclusion bodies in spinal cord and cortex (note: nigra absent of pathology). Motor impairment assayed by rotorod.		Giasson, et al. Neuron 2002; 34:521-533.
Human α-synuclein: A53T	Murine PrPC3H/HeJ x C57BL6/J backcrossed into C57Bl6/J	α-syn inclusions, progressive motor impairment.		Lee, et al, in press
Human α-synuclein: WT and A53T	Thy1C57Bl/6	α-syn inclusions, progressive motor impairment.		Sommer, et al. Exp Geront 2000; 35:1389-1403.
Human α-synuclein: A53T				Nussbaum, in press?
Human Tau:P301L	Murine PrPC57BL/DBA2/SW	Neurofibrillary tangles and Pick-body-like lesions, tau-immunoreactive pre-tangles in the cortex, hippocampus and basal ganglia. motor and behavioural deficits.		Lewis et al. Nat Genet 2000;25(4):402-5.
α4 nicotinic receptor knock-in α4 nicotinic receptor		These mice have a severe deficit of dopaminergic neutons in the substantia nigra.The viable mice display increased anxiety, poor motor learning, excessive ambulation that is eliminated by very low levels of nicotine, and a reduction of nigrostriatal dopaminergic function upon aging.		S Orb et al. Physiol. Genomics 2004: 18, 299-307 [abstract]; H. Lester et al., Current Opinion in Drug Discovery & Development, 2003: 6(5), 633-639 [abstract]; C. Labarca, et al., PNAS, February 27, 2001: 98(5), 2786-2791 [abstract].

Last updated March 16, 2005