FIGURE 6.

αS pathology is not associated with inhibited complex I activity. Representative images of immunohistochemistry analysis of A53T αS tg mouse brains aged 12–15 months. Formalin-fixed tissue immunostained with anti-αS antibody (Syn 303) and visualized with diaminobenzidine as chromogen (see “Materials and Methods”). a–d, Nontransgenic (a), transgenic brain stem (b), transgenic substantia nigra (c), and transgenic cerebellum (d). αS staining appears throughout the cell body with some Lewy neurites and Lewy bodies (arrowheads). e, quantitation of total αS immunoreactivity (including pathogenic and normal expression) in the brain stem of young (4–6 weeks) and old (12–15 months) A53T αS mouse brains. The values are the means of n = 5–6 brains and 3–4 images for each mouse brain ± S.D. *, t test, p < 0.05. f, insoluble, lipid associated-αS in young (4–6 weeks old) and old (12–15 months old) A53TαS tg mouse brains. Chloroform/methanol extraction of a sample of the lipid-rich low speed fraction (50 μl of total 500 μl of suspension) of young and old A53T αS mouse brains. The interface between the organic (lower part) and aqueous (upper part) fractions was resuspended in 2× Laemmli buffer, analyzed by 10% Tris-glycine PAGE, and blotted with LB509. g, quantitation of αS immunoreactivity in f presented as the ratio between the high molecular weight immunoreactive species to monomer in the same lane.