Fig. 1: GCase activity and level measured in LRRK2 G2019S KI mice brains. | npj Parkinson's Disease

Fig. 1: GCase activity and level measured in LRRK2 G2019S KI mice brains.

From: LRRK2 kinase activity regulates GCase level and enzymatic activity differently depending on cell type in Parkinson’s disease

Fig. 1

a GCase activity measured in brain extracts from different brain regions (midbrain, cortex and striatum) shows limited differences between WT and GSKI brains, while the difference is significant across the different measured tissue extract (n = 4–5 samples per genotype, two-way ANOVA test, p = 0.015, F(2, 21) = 9.013 for brain regions; p = 0.0708, F(1, 21) = 3.623 for genotype; data are expressed as mean ± SEM). b Western blot analysis of GCase protein levels and the relative β-actin loading control of tissue extracts from the midbrain for WT and KI mice. c Quantification of GCase protein level normalized to β-actin showed a significant decrease in GSKI midbrain compared with WT tissue extracts (n = 4–5 samples per genotype, Student t test, two-tailed ****p < 0.00001, Shapiro–Wilk normality test; data are expressed as mean ± SEM). d Quantification of GCase at the mRNA level via qPCR, using the housekeeping gene PPID (peptidylprolyl isomerase D), in GSKI midbrain compared with WT showed no significant difference between the two (n = 4–5 samples per genotype, two-way-ANOVA, p = 0.0353, F(2, 21) = 3.936 for genotype; p = 0.0580, F(1, 21) = 4.020 for mouse age; Tukey’s multiple comparison test indicates no differences between genotypes at the same age; data are expressed as mean ± SEM). e GCase activity was significantly higher in GSKI mice tissue when normalized to the GCase level (n = 4–5 samples per genotype, Student t test, two-tailed p = 0.0099, Shapiro–Wilk normality test; data are expressed as mean ± SEM).

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