Skip to main content
Fig. 4 | Molecular Neurodegeneration

Fig. 4

From: Tau oligomers mediate α-synuclein toxicity and can be targeted by immunotherapy

Fig. 4

Lewy body-like structures are significantly decreased in TOMA-treated A53T mice. a α-synuclein structures were detected by immunofluorescence with LB509 (red) and nuclei were labeled with DAPI (blue). b Control IgG-treated mice had a significantly higher ratio of Lewy body-like structures to total nuclei when compared to TOMA-treated mice (p = 0.039). c Levels of soluble α-synuclein oligomers detected by ELISA with Syn33 were significantly elevated in both Control IgG and TOMA-treated A53T mice compared to wildtype mice (p < 0.0001) d PBS insoluble oligomeric α-synuclein was significantly increased in A53T mice treated with TOMA and Control IgG (p < 0.0001), however TOMA-treated mice had significantly decreased α-synuclein oligomers compared to Control IgG mice (p < 0.0001). e TOMA-treated mice had significantly higher soluble α-synuclein oligomers detected with (f) F8H7 (g) and Syn33 and (h) a trend toward lower phosphorylated α-synuclein by Western blot. i TOMA-treated mice showed elevated levels of α-synuclein oligomers detected with Syn33 over Control IgG approaching significance (p = 0.059; left panel), but PK-resistant α-synuclein oligomers were found to be significantly increased in Control IgG mice compared to TOMA (p = 0.036; right panel). j-k Levels of total α-synuclein detected by ELISA with 4D6 were unchanged in both soluble and insoluble fractions of total brain homogenate. l No differences were detected in total α-synuclein levels measured by fluorescence intensity (ratio to nuclei) with 4D6 between TOMA and Control IgG treatment groups. Scale bar 20 μm. TOMA (n = 6), Wildtype (n = 6), Ctrl IgG (n = 8)

Back to article page
\