The A53T alpha-synuclein transgenic mice were developed by and generously provided by Dr. Virginia Lee, University of Pennsylvania. These transgenic mice (B6;C3H-tg(Prnp-SNCA)M83/Vle, updated in 2010 to B6;C3H-Tg(Prnp-SNCA*A53T)83Vle) carry a transgene expressing a mutant form of alpha-synuclein, producing a motor deficit in early adult life. The background for this line is a mixture of C57BL/6 and C3H. The NIA Mutant Mouse Aging Colony will backcross the transgene onto C57BL/6 background (to be available later), but the publications to date have used the transgene on the mixed background so we will keep this background available as well. The mice are homozygous for the transgene, which results in earlier expression of the phenotype than was observed in hemizygotes.
The motor deficit manifests at about 7-12 months of age and the mice deteriorate rapidly. Mice with a severe impairment will be euthanized for humane reasons so availability at older ages will be very limited.
Giasson BI, Duda JE, Quinn SM, Zhang B, Trojanowski JQ, Lee VM. Neuronal alpha-synucleinopathy with severe movement disorder in mice expressing A53T human alpha-synuclein. Neuron. 2002 May 16;34(4):521-33.