Fig. 8

L-DL improves cognition in AD mice via modulating alternative splicing and expression of synaptic genes. a, b Alternative splicing products of CAMKV, determined by RT-PCR (a) and densitometric analyses (b) in the hippocampus of APP/PS1 mice with control or L-DL OE (n = 3 per group). c, d Alternative splicing products of CAMKV, determined by RT-PCR (c) and densitometric analyses (n = 3) (d) in the hippocampus of APP/PS1 mice with control and L-DL KD (n = 3 per group). e, f Protein levels of CAMKV, SNAP25, PSD95, NR2B in the hippocampus of APP/PS1 mice with control or L-DL OE (n = 3 per group), determined by immunoblotting (e) and densitometric analyses (f). GAPDH was included as an input control. g, h Protein levels of CAMKV, SNAP25, PSD95, NR2B in the hippocampus of APP/PS1 mice with control or L-DL KD (n = 3 per group), determined by immunoblotting (g) and densitometric analyses (h). GAPDH was included as an input control. Statistical analysis was performed using two-tailed Student’s t-test; * P < 0.05, ** P < 0.01, *** P < 0.001; error bars denote SEM