Fig. 8

Intravenous delivery of glunomab reduces neuroinflammation and DA-neuron degeneration and rescues behavioral deficits after overexpression of hα-SYN. Representative images of the SN stained for (A) TH and (C) MHC-I, and the respective quantification of (B) DA-neuron survival and (D) MHC-I fluorescence intensity fold change in the SN 4 weeks after rAAV2-hα-SYN injection in WT mice treated with glunomab (10 mg/kg/week) or vehicle (n = 6–10). (E) Confocal image of the SN showing CD3⁺ cells (red) in contact with TH⁺ cell bodies and axons. (F) Quantification of CD3⁺ T cells associated with the SNpc 4 weeks after rAAV2-hα-SYN in WT mice treated with glunomab or vehicle (n = 7–10). (G) Quantification of sensorimotor bias in a corridor task 4 weeks after rAAV2-hα-SYN in WT mice treated with glunomab (10 mg/kg/week) or vehicle (n = 9–10). Glunomab treatment was performed on 12- and 16-week-old WT mice. For vehicle treatment, age-matched 12- and 16-week-old WT mice were used. Data are shown as mean ± SEM, N.S = not significant, *p < 0.05; ****p < 0.0001. (B, F, G) 2-tailed t-test; (D) 1-way ANOVA followed by Tukey post hoc test. Scale bar= (A, C) 250 μm (E) 20 μm