Research Paper Volume 9, Issue 5 pp 1386—1403

Transgenic autoinhibition of p21-activated kinase exacerbates synaptic impairments and fronto-dependent behavioral deficits in an animal model of Alzheimer’s disease

Figure 2. Consequences of the long term inhibition of PAK in 18-month-old 3xTg-AD mice on AD neuropathology markers. (A) PAK inhibition did not affect Aβ accumulation in frontal cortex, suggesting a downstream position for PAK in Aβ pathological cascade. (B) Reduced PAK activity in 3xTg-AD-dnPAK animals led to a higher proportion of tau phosphorylated at Ser202/Thr205 (CP13) and Ser396/Ser404 (AD2) in detergent-insoluble fraction but had no effect on the phospho-epitope Thr181 (AT270). Data expressed as means ± SEM over total human tau (tau-13) (p<0.05, one-way ANOVA, Tukey-Kramer post hoc, O p<0.05, student t-test).