Pan-neuronal expression of K_v4 slows the onset and severity of Aβ42-induced neurodegeneration.

<p>(A) Representative confocal images, from MB position described in <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005025#pgen.1005025.g007" target="_blank">Fig. 7</a>, show nuclear (DAPI) staining (upper panels, blue) from five genotypes, including <i>UAS- Aβ42/+</i> (Ctr), <i>elav-GAL4;UAS-Aβ42/+</i> (Aβ42), <i>elav-GAL4;UAS-Aβ42/UAS-K</i>_<i>v</i><i>4</i> (Aβ42+K_v4), <i>elav-GAL4;UAS-Aβ42/UAS-GFP</i> (Aβ42+GFP) and <i>elav-GAL4;UAS-Aβ42/UAS-K</i>_<i>v</i><i>1</i> (Aβ42+K_v1). Co-immunolabeling for Aβ42 is shown (lower panels, red) from these genotypes. Brains were dissected and labeled from flies aged 15 days (15d), 25 days (25d) and 40 days (40d) AE. Note that Aβ42 immunostaining is clearly seen in all the genotypes except Ctr. (B) Quantification of cell density (DAPI-positive) from confocal images described in (A). Note that there is significant cell loss in Aβ42, Aβ42+GFP, and Aβ42+K_v1 flies at 25d, but not in Aβ42+K_v4. n = 6–8 for each genotype, * P < 0.05, ** P < 0.01, *** P < 0.001, Student’s t-test. (C) Relative anti-Aβ42 signal was quantified in the same aged genotypes described in (A); background fluorescence is reflected in Ctr samples. Note that no significant difference in Aβ42 signal was seen in Aβ42+K_v4 brains, compared to Aβ42 at 15 and 25 days AE; at 40d AE, Aβ42+K_v4 brains show an increase in Aβ42 signal; quantification, however, was difficult due to the number of degenerative “holes” seen in confocal sections at this age. n = 6–8 for each genotype. All data are expressed as means ± SEM.