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. 2022 Dec 1;17(12):e0277532. doi: 10.1371/journal.pone.0277532

Fig 5. Treatment with the SCD inhibitor CAY10566 reversed the abnormal fatty acid profiles and pathogenic α-synuclein levels.

Fig 5

A and B) C16 and C18 desaturation index (DI) and essential fatty acids Linoleic (C18:2n6) and γ-Linolenic acid (C18:3n6) from A53T/Corr neurospheres (A) and S3/KD neurospheres (B) treated for 2 weeks with 0.03% DMSO and 0.3 μM CAY10566. Data are from three independent neurosphere differentiations, with two biological replicates per differentiation, total 6 biological replicates. All values in each differentiation were normalized to the isogenic control groups treated with DMSO in each respective batch of differentiation. C and D) Representative Western blot (top panels) and quantification (bottom panels) for pS129 and total α-synuclein in 54-day-old cortical neurospheres from A53T/Corr (C) and S3/KD (D) treated for 2 weeks with 0.03% DMSO and 0.3μM CAY10566. Quantification includes data from three (A53T/Corr) and two (S3/KD) distinct differentiations with two biological replicates per group in the S3/KD neurosphere differentiations (total 4 biological replicates). Data is mean ± standard deviation and analyzed by One-way ANOVA analysis with Tukey’s multiple comparison test. (*P<0.05; **P<0.01; ***P<0.005; ****P<0.0001).