Fig. 5
Rescue of disrupted cathepsin maturation and activity in mice overexpressing αSyn A53T in dopaminergic neurons. a Western blot analysis of αSyn detected with C-20 antibody in thalamus/midbrain Triton-soluble samples of non-transgenic (ntg) mice and mice overexpressing human A53T in dopaminergic neurons (DAsyn53). DAsyn53 mice were treated with FTI for 26 days. b Quantification of αSyn signal intensities of ntg, DASYN53 and FTI-applied DASYN53 mice. Each αSyn signal (detected with C-20 antibody) was normalized to the corresponding GAPDH signal and displayed as fold change, compared to vehicle ntg mice (n = 5). c Representative Western blot analyses of thalamus/midbrain samples of ntg, DAsyn53 and DAsyn53 mice treated with FTI stained for CTSD, CTSL as well as CTSB. d Corresponding quantifications of Western blot analyses of mature forms (heavy chain, hc) of CTSD (left), CTSB (middle) and CTSL (right). Signal intensities were normalized to β-actin signals and expressed as fold change, compared to ntg (n = 3–5). e Enzymatic activity assay for CTSD, CTSB, and CTSL in whole lysates from thalamus/midbrain mouse brain samples (n = 3–4). Statistical analyses were performed by using one-way ANOVA together with Tukey’s multiple comparison test. ***P < 0.001, **P < 0.01, *P < 0.05