The A30P mutation of the human SNCA gene has been linked to familial Parkinson’s disease. These mutant mice carry a transgene containing a human SNCA gene with the A30P mutation and a knock out allele of the mouse Snca gene. Western blot analysis of brain tissue reveals human &alpha;-synuclein protein at levels significantly lower than endogenous wildtype C57BL/6 mouse &alpha;-synuclein protein levels. The transgene expression pattern is similar to the endogenous mouse Snca expression pattern. The transgene was detected at a single site of integration near the telomere on one copy of chromosome 15 by fluorescence in situ hybridization analysis. Electrically evoked dopamine release is reduced in the striatal caudate putamen, but not in the nucleus accumbens, of SNCA-A30P mice, when compared to Snca KO mice. Mutant mice exhibit increased anxiety with age and an increase in activity during the dark phase of a 12 hour- 12 hour light-dark cycle. Mice that are homozygous for the targeted mutation and hemizygous for the transgene are viable and fertile. The Donating Investigator has not attempted to make the strain homozygous for the transgene but reports double homozygous animals should be viable.

These SNCA-A30P mice express a transgene containing a mutant human SNCA gene and are suitable for use in applications related to the study of Parkinson's disease.

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B6.Cg-Snca<tm1Rosl> Tg(SNCA*A30P)192Rwm/J Frozen Embryo