Fig. 7
Altered lipid homeostasis in oligodendrocytes drives α-synuclein aggregation in vivo. a Levels of total hexosylceramide (HexCer) species in whole brain homogenates from 6-month-old Gba1f/f and Gba1f/f::cre mice (**, p < 0.01; unpaired two-tailed Student’s t-test; n = 4). Error bars indicate s.d. b, c Representative immunofluorescence images for Triton X-100-insoluble α-synuclein and MBP in the corpus callosum from 6-month-old Gba1f/f and Gba1f/f::cre mice (b) and relative quantification of the number of puncta detected per field (Unpaired two-tailed Mann–Whitney test; n = 4 mice). Error bars indicate s.e.m. CC, corpus callosum, Str, striatum. Scale bar = 50 μm. d-f Representative western blot of α-synuclein monomer and oligomers (e) in total brain protein extracts from 6-month-old Gba1f/f and Gba1f/f::cre mice and relative densitometric quantification (e, f). β-actin (ACTB) was used as loading control. Lower and higher exposure are shown to highlight the presence of oligomers as well as of the monomer (*, p < 0.05; unpaired two-tailed Student’s t-test; n = 15 mice for α-synuclein monomers and n = 12 for α-synuclein oligomers). Error bars indicate s.e.m