hA53Ttg α-synuclein transgenic mice express A53T mutant human α-synuclein under the control of the murine Thy-1 promoter.
The onset of motor deficits in hA53Ttg mice can be observed as early as 2 months of age as analyzed with the beam walk test. Motor deficits in the RotaRod test are significant starting at the age of 4 months. Severe muscle strength deficits in hA53Ttg mice can be observed already at the age of 2 months. These deficits do not further increase with age. Orofacial deficits in the pasta gnawing test are measurable only at the age of 4 months.
Figure 1: Motor deficits in the beam walk and RotaRod test of hA53Ttg mice compared to non-transgenic littermates. Time to traverse the beam (A) and number of slips (B) in the beam walk test as well as time to fall off the rod in the RotaRod test (C). n = 23-24 per group. Two-way ANOVA with Bonferroni’s post hoc test; mean + SEM; ***p<0.001.
Figure 2: Muscle strength and motor deficits in the wire hanging test and pasta gnawing test of hA53Ttg mice compared to non-transgenic littermates. Wire hanging time observed in the wire hanging test (A) and bites per episode in the pasta gnawing test (B). n = 23-24 per group. Two-way ANOVA with Bonferroni’s post hoc test; mean + SEM; **p<0.01; ***p<0.001.
QPS Neuropharmacology offers a custom-tailored study design for this model, and we are flexible to accommodate to your special interest. hA53Ttg mice show relevant features of Parkinson’s disease already at young age. This allows for extraordinarily fast turn-around times.
We would be happy to test your compounds in the hA53Ttg mouse model! The most common readouts are:
- Muscle weakness and motor deficits
- α-synuclein expression levels
- Reduced anxiety