Figure 3. Altered neurological status of ATXN1[30Q]-D776 mice.
(A) Accelerating Rotarod performance on day four at 6 and 12 weeks-of-age.
ATXN1[30Q]-S776/S776 (homozygous) mice, at 6 and 12 weeks (n = 9), were compared to age-matched wt/FVB mice, at 6 and 12 weeks (n = 10). ATXN1[30Q]-D776 mice at 6 weeks (n = 5) and at 12 weeks (n = 14), compared to age-matched littermate wt/FVB mice at 6 weeks (n = 9) and at 12 weeks (n =12; *p = 0.025 and **p = 0.0008, student t-test, two tailed equal variance). Performance of ATXN1[82Q]-S776 mice, at 6 weeks and 12 weeks (n = 15), compared to age-matched littermate wt/FVB mice, at 6 weeks and at 12 weeks (n = 8; *p = 0.006 and **p = 0.0005, student t-test, two tailed equal variance).
(B) ATXN1[30Q]-D776 mice (n = 9, *p = 0.008 student t-test, two tailed equal variance) show a similar gait performance defect as ATXN1[82Q]-S776 mice (n = 20, **p = 0.005 student t-test, two tailed equal variance) compared to age-matched littermate wt/FVB mice (n = 9 &16, respectively) as assessed by hind stance width at 12 weeks-of-age.
(C) Four day trial of accelerating Rotarod performance of mice at 30 weeks-of-age. Both ATXN1[30Q]-D776 (n=3) mice and ATXN1[82]-S776 (n=4) at 30 weeks-of-age were compared to age-matched wt/FVB (n=3) (p=0.04 and p=0.03).