FapCS accelerated Aβ‐induced cognitive and neuronal pathology in adult zebrafish. Aβ (1 µL, 40 × 10−6m) was injected to the cerebroventricular space of 10 months old adult zebrafish. A) Representative movement trajectories of adult fish after injection with FapCS, Aβ, or Aβ + FapCS. B) The quantitative measurements of movement frequency and total distance traveled by the fish (n = 3 per group and three groups per sample). Aβ + FapCS significantly suppressed (**, p < 0.005) the swimming behavior of adult fish, compared to Aβ alone at 4 d posttreatment. C) Cognitive memory function of the adult fish. The swimming tank was divided into arenas 1 and 2. Arena 2 was labeled with red paper from the bottom and fish was trained to avoid swimming into arena 2. The fish was shocked (9 V) whenever it swam into arena 2. D) Quantitative measurement of movement frequency and distance traveled in arena 1 versus arena 2. Before training, fish were able to freely swim in both arenas and no difference per arena was observed. After training, buffer injected and Aβ (4 d postinjection) fish were able to cognitively avoid swimming into arena 2. However, FapCS + Aβ and Aβ alone at 4 d and 2 weeks postinjection, respectively, were unable to avoid arena 2 and no significant difference in the swimming activities was observed in arena 1 versus arena 2 (n = 3 per group and 3 groups per sample). E) IHC for Aβ deposition in the brain of zebrafish. F) Quantitative measurement of green fluorescence for antibody staining (n = 3). G) Synaptophysin positive cells, H) quantitative measurement of anti‐synaptophysin antibodies labeling (n = 3), I) TUNEL assay and J) quantitative measurement for antibodies labeling in TUNEL assay (n = 3). Aβ alone at 2 weeks and Aβ + FapCS at 4 d presented a similar level of Aβ burden, neurodegeneration of synaptophysin positive cells and neuronal cell death in the fish brain, that were significantly different (**, p < 0.005) than Aβ alone at 4 d postinjection.
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