Fig. 1

TgM83^+/− mice subjected to MCAO gain weight but develop motor deficits within 180 days. TgM83^+/− mice expressing the A53T mutant of human α-synuclein were subjected to middle cerebral artery occlusion (MCAO) for 30 min or sham surgery without occlusion of the artery. Groups of treated animals were sacrificed at 14, 30, 90, 180, and 360 days post surgery and neuropathology was analyzed by histology and biochemistry (a). Additionally, the motor behavior of treated animals was tested at 90, 180, and 360 days post surgery on a rotarod treadmill (a). TgM83^+/− mice subjected to MCAO (n = 8, red lines) as well as sham-treated animals (n = 6, blue lines) gained body weight until the end of the experiment at 360 days post surgery (b). MCAO- and sham-treated mice were tested for motor impairment using a rotarod at 90, 180, and 360 days post surgery. TgM83^+/− mice that had been subjected to MCAO (red) showed significantly reduced motor skills at 180 and 360 days post surgery relative to 90 days post surgery (c). In contrast, sham-treated control animals (blue) did not develop any motor deficits. Six to ten animals were analyzed per group. The data represents the mean latency to fall in seconds ± standard error of the mean. P values were computed using two-way ANOVA followed by Tukey’s post-hoc test (P: * < 0.05, ** < 0.01)