Fig. 1.

Pathological α-synuclein oligomers are associated with inflammatory responses in A53T mouse striatum. a TNFα (**P = 0.0029), IL-1β (***P = 0.0003), IL-10 (***P = 0.0001) and IFNγ (^#P < 0.0001) levels in striatal homogenates determined using cytokine-specific ELISA assays (N ≥ 4 per genotype). b, c Representative western blots of CHAPS-homogenized striatum using antibodies against total (anti-Syn1) and phosphorylated α-synuclein. d Immunoblots of mouse IgG heavy chain and densitometric quantification in WT (n = 16) and A53T Tg (n = 14) mice, ^#P < 0.0001. e–g Correlation analysis of mouse IgG light chain in A53T Tg mice with α-synuclein oligomers (e), α-synuclein monomers (f), and animal age (g) after immunoblotting and densitometric quantitation (n = 10). h–j Western blotting of homogenized striatal tissues from 1.5-month-old WT and A53T Tg mice (n = 4 mice per genotype) using antibodies against total α-synuclein (anti-Syn1) and densitometric quantification of monomeric α-synuclein levels (i, **P = 0.0019) and IgG levels (j, P = 0.7219). A six-month-old A53T Tg homogenate was used as reference for the presence of α-synuclein oligomers. k Representative immunoblots and quantification of C3d (n = 4 mice per genotype, **P = 0.0074). In b–d, h and k, GAPDH was used as a loading control. Statistics by Mann–Whitney test in (d) and unpaired Student’s t test in (a, i, j, k)