Fig. 5

Mitigation of Aβ toxicity in zebrafish larvae with βCas AuNPs. a Aβ peptide was injected into the cerebroventricular space at 10, 50, and 100 fM concentrations (n = 20, mean ± SD). Zebrafish larvae were monitored on an automated behavior monitoring system at fifth day post Aβ treatment and parameters of total distance traveled, movement frequency and trajectory path were observed for 1 h. Significant (p < 0.005) difference in the behavior of the larvae was observed on the fifth day post treatment. βCas AuNPs injected, via the intracardiac route 2 and 6 h after the Aβ treatment, rescued the larvae from Aβ toxicity and from developing Alzheimer’s-like symptoms. Representative trajectories of the larvae are displayed in the far-right column. Treating the larvae with βCas AuNPs, 12 and 24 h post Aβ treatment, failed to protect the larvae from developing Aβ toxicity. b Zebrafish larvae, treated with βCas AuNPs 2 h after Aβ treatment were fixed, sliced and stained with Congo red to image any Aβ fibrils that could have formed. Tissue slices of the brain section did not present any red fluorescence, indicating no Aβ fibril formation in βCas AuNPs treated larvae (scale bars: 200 µM; inset scale bar: 20 µM). Furthermore, immunohistochemistry (IHC) (c) and polarized light microscopy (apple green birefringence of amyloid) (d) revealed deposition of aggregated Aβ in the larval brain while no Aβ deposition was observed in βCas AuNPs or buffer treated larvae (Scale bars: IHC, 30 µM; polarized light microscopy, 50 µM). Error bars represent the standard deviation