Curcumin affects the brain amyloid deposition histology patterns as a function of <i>Drosophila</i> genotype.

<p>Micrographs of <i>Drosophila</i> brains taken with 100× objective showing fluorescence from cell nuclei by DAPI (blue), amyloid aggregates by p-FTAA (green) and Aβ by αAβ-antibody (red). (A–E) Control flies with and without treatment with curcumin at day 0, day 10, and day 20, showed no antibody or p-FTAA binding species in the brain tissue. (F–J) Double insert Aβ_1–42 expressing flies showed extensive amyloid staining by p-FTAA, with several long extended fibrillar aggregates at all time points. Curcumin treatement accelerated p-FTAA positive (amyloid aggregate) conversion at young age (c.f. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0031424#pone-0031424-g003" target="_blank">Figure 3G and H</a>). The amount of detectable aggregates increased with age. DAPI staining from regions with widespread p-FTAA-positive aggregates were decreased. (K–O) Aβ_{1–42 E22G} expressing flies at day 0, day 5, and day 10, showed a spot-like staining from both p-FTAA and the Aβ specific antibody, but a weaker p-FTAA staining was apparent (c.f. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0031424#pone-0031424-g003" target="_blank">Fig. 3 I and N</a>). Some irregular nuclei were visible from the DAPI staining. Day 0 and day 5 flies showed protein aggregates detectable with the antibody and to some extent by p-FTAA. The same staining pattern was reveled irrespective of curcumin treatment. Filled arrowheads show p-FTAA positive amyloid aggregates and open arrows indicate αAβ-antibody positive aggregates (diffuse Aβ accumulation). Scale bars in insets represent 20 µm.