Fig. 8.

Female tau mice show deficits in motor coordination and motor learning. Top row (a, d, g) Latency to stay on the accelerating RotaRod in Trial 1 and 2 as an index for motor coordination. L1 mice (g 5–6 months; WT n = 14; L1 n = 14) were significantly impaired, as were homozygous L66 (d 6 months; WT n = 24, L66^+/− n = 14; L66^+/+ n = 13; L66^+/+ dysk. n = 12), but not L66 aged 4–5 weeks (a WT n = 40; L66 n = 34). Heterozygous L66 did not present with a phenotype up to 6 months. Middle row (b, e, h) Motor learning on the RotaRod over 12 trials (3 days of 4 trials) was impaired in all transgenic cohorts including L1 (h), as well as homo- and heterozygous L66 at 4–5 weeks (b) or 6 months (e). Bottom row (c, f, i) Overall performance gain between trial 1 and 12 in different cohorts. Despite a performance deficit in L1, the overall amount of improvement was not different to controls (i). Similarly, all L66 cohorts had significant learning different from 0 (not indicated), but L66 mice typically improved less than WT both at 4-weeks (c) and 6 months (f). Values expressed as mean ± SE; asterisks denote group differences (Student’s t test) at p < 0.05