Fig. 1

Localization and demonstration of the beneficial effects of aggregated Aβ1–42 on P. acuticornis. Juvenile rotifers were selected in different groups after 1-day starvation: fed (a; 12 days normal feeding), unfed (b; 12 days starvation) and Aβ1–42 treated (for 12 days). The Aβ1–42 in the digestive system (stomach and intestine) of live rotifers were visualized by fluorescent Bis-ANS (c; green colour in the representative photograph; 3 h = aggregated for 3 h) and absorbent Congo red (d; red colour in the representative photograph; 3d = aggregated for 3 days). Untreated individuals labelled with these two dyes showed no signal (not shown). e The normalized mean lifespan (NML) of the Aβ1–42-treated animals was significantly longer than that of their normally fed and unfed untreated controls, with a significant difference between the 3 h- and 3d–aggregated forms. Besides NML, four viability markers were measured, including body size index (BSI), bright light disturbance (BLD), mastax contraction frequency (MCF), and cellular reduction capacity (CRC). The Aβ1–42-treated rotifers performed significantly better than their unfed untreated controls and there were significant differences between the subgroups treated with two the differently aggregated forms in BSI and CRC. The concentration of Aβ1–42 was 100 μg/mL; n = 30 (NML), 50 (BSI), 20 (BLD), and 24 (MCF) one-housed individual rotifers per group; n = 24, well with normalized absorbance to rotifer number (CRC). The scale bars in the proportional representative photographs represent 20 μm (*, significant difference from the fed and Aβ1–42-treated groups; #, significant difference from the group treated with the 3 h aggregated form). The possible distribution of the exogenous Au-Aβ1–42 complex was studied in vivo with SEM in the body of P. acuticornis: f rotifer without treatment (background); g Au-Aβ1–42-treated rotifer. Homogenously signals of gold can be detected in Au-Aβ1–42-treated entities. Scale bar represents 10 μm