FapCS accelerated Aβ fibrillization and associated pathology in zebrafish larvae. Aβ (100 × 10−15m), FapCS (10 × 10−15m) or Aβ + FapCS at a 10:1 molar ratio (100:10 × 10−15m) were injected to the cerebroventricular space of one week old zebrafish larvae. Congo red (100 × 10−15m) was injected at 2 d or one week post Aβ injection to stain and monitor the Aβ fibrillization. A) The fluorescence images recorded via the brightfield and red fluorescence channel of a microscope for the whole‐mount dorsal and lateral side of larvae. B) Quantitative measurement of the relative red fluorescence intensity, indicative of Congo‐red‐stained Aβ plaques, from the cerebral region of larvae (n = 10). Aβ injected together with FapCS presented significantly stronger (**, p < 0.005) fluorescence and thus elevated Aβ fibrillization compared to Aβ alone or buffer, at 2 d postinjection. FapCS did not show any retention of Congo red fluorescence in the brain. C,D) Aβ‐induced behavioral pathology in terms of movement frequency (C) and total distance traveled by zebrafish larvae (D) (n = 10 per group and three groups per sample). The measurements were made for the observation period of 1 h at 2 d and one week postinjection. FapCS significantly aggravated (**, P < 0.005) Aβ toxicity and reduced the movement frequency and total travel distance of the larvae at 2 d postinjection. E) ROS generation in the brain homogenates of zebrafish larvae presented as relative DFC fluorescence. H2O2 was used as positive control. Similar to behavioral toxicity, Aβ + FapCS significantly enhanced ROS production in the larval brain (n = 10 per group and 3 groups per sample).
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