Fig. 9

Timeline of pathogenesis in the CNS of TgM83^+/− mice after ischemic stroke. Ischemia-induced astrogliosis (orange line) and microgliosis (pink line) both peaked at 14 days after the initial insult, which is also when α-synuclein aggregation (blue line) steadily began to increase based on FRET analysis. Astrogliosis and microgliosis returned close to their pre-ischemic levels by 90 and 180 days post ischemia, respectively, while α-synuclein aggregation continued to increase. Possibly due to the gradually increasing load and deposition of aggregated α-synuclein in the brain, a second inflammatory process set in with a renewed increase in astrogliosis that was slowly followed by microgliosis. By 180 days post ischemia, when cellular deposits of pathologic α-synuclein were first detected, animals also showed first symptoms of motor disease (black line), which worsened over time. By 360 days post ischemia a loss of dopaminergic neurons was detected in the ipsilateral side of the substantia nigra (red line)