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. Author manuscript; available in PMC: 2021 Oct 5.
Published in final edited form as: Cell. 2021 Apr 13;184(10):2715–2732.e23. doi: 10.1016/j.cell.2021.03.032

Figure 3. Low-dose salsalate-mediated inhibition of p300/CBP acetyltransferase protects mice from post-TBI-induced elevated ac-tau, AIS degradation, tau mislocalization, neurodegeneration, and cognitive deficits.

Figure 3

(A) Low-dose salsalate dose-dependently reduces post-TBI elevations in ac-tau in the brain (n = 3, *p < 0.05, **p < 0.01, ***p <0.001 versus TBI-+Vehicle group, one-way ANOVA; and Tukey’s post hoc analysis).

(B) Low-dose salsalate protects mice from post-TBI AIS degradation (scale bar, 5 μm).

(C) Low-dose salsalate protects mice from post-TBI tau mislocalization (scale bar, 5 μm).

(D) Low-dose salsalate protects mice from post-TBI axonal degeneration (scale bar, 5 μm). In (BHD), each group n = 3, *p < 0.05, **p < 0.01, ***p <0.001, ****p < 0.0001 versus TBI+Vehicle group, one-way ANOVA and Tukey’s post hoc analysis.

(E) Low-dose salsalate protects mice from post-TBI impairments in motor (foot slip assay) and cognitive (learning and memory in the Bames maze) behavioral assays. (*p < 0.05, **p < 0.01, ***p<0.001, ****p < 0.0001 versus TBI+vehicle group, repeated-measures two-way ANOVA (learning) and one-way ANOVA (memory) and Tukey’s post hoc analysis.

See also Figures S5 and S6.