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. 2021 Jul 7;4:843. doi: 10.1038/s42003-021-02218-7

Fig. 7. Carnosine and kynurenic acid protect against Aβ42 aggregation and toxicity in an HSF-1-dependent manner.

Fig. 7

a RNAi knockdown of hsf-1 shows decreased motility in GMC (AD) worms. L4440 is the empty vector control. On treatment with carnosine and kynurenic acid, a significant increase in motility is observed in the L4440 phenotype as compared to a decrease in the hsf-1(RNAi) groups. The control N2 worms show no significant effect of the metabolites carnosine (Car) and kynurenic acid (Kyn). The radar chart depicts overall fitness by comparing the three quantitative variables: worm speed (mm/s), bends per minute and live ratio as is seen on its axis. The bar graph inset shows that RNAi knockdown of hsf-1 significantly impairs the beneficial effects of carnosine and kynurenic acid. Statistics were performed using one-way ANOVA, Dunnett’s multiple comparisons test against the untreated Aβ42 empty vector. ****p < 0.0001; ***p < 0.001; **p < 0.01; *p < 0.05 (b). A corresponding decrease in NIAD-4 aggregates is observed in AD worms treated with carnosine and kynurenic acid (Scale bars, 80 μm). For NIAD-4 staining, approximately 11–30 animals were analyzed per condition. All error bars represent SEM. Statistics were performed using one-way ANOVA Dunnett’s multiple comparisons test against the untreated Aβ42 empty vector. ****p < 0.0001; ***p < 0.001; **p < 0.01; *p < 0.05. c Representative images of Aβ42 plaques show a significant clearance of aggregates in worms treated with carnosine (Car) and kynurenic acid (Kyn). hsf-1 knockdown worms even when treated with carnosine and kynurenic acid did not clear aggregates. White arrows point to NIAD-4-stained Aβ42 aggregates, which appear orange-red in color. For comparison, an empty RNAi vector L4440 GMC worm head is shown.