Abstract
Abhik Sen, Thomas J. Nelson, Daniel L. Alkon and Jarin Hongpaisan
[Journal of Alzheimer’s Disease, 63(3) (2018) 1173-1189, DOI 10.3233/JAD-171008]
http://doi.org/10.3233/JAD-171008
On page 1186, in Figure 8a, the empty area outside the tissue section at the right side was filled with part of Wild panel, due to the mistake of copying and pasting Tg image over the Wild image during image preparation. In addition, the wild panel in Figure 8C was accidentally taken from the same original image of and overlapped with Tg + Bry panel during the figure preparation process. The Wild panel in Figure 8C was then replaced. This erratum does not change the results and conclusions of the paper. The corrected Figure 8 and caption are provided below.
An inverse correlation between PKCɛ and Aβ and effect of PKCɛ activation on MnSOD level in hippocampal neurons from Tg2576 transgenic AD mice. Tg2576 (Tg) and wild-type (Wild) control mice at 8 weeks of age were treated with or without the PKCɛ activator bryostatin (Bry, 30μg/kg, ip, 2 times per week) for a 12-week period. (A) Immunohistochemistry and confocal microscopy demonstrated (B) an inverse correlation between Aβ and PKCɛ in mossy fibers. Data are represented as mean, n = 9 mice per condition and 3–4 measurements per mouse (C) Immunohistochemistry showed that (D) the reduction of MnSOD was prevented with bryostatin 1 in the cell bodies of the CA1 hippocampal pyramidal neurons. Data are represented as mean±SEM, n = 3 mice (59–70 neurons per mouse). Data were divided by DAPI (4’,6-diamidino-2-phenylindole) staining, ***p < 0.005; one-way ANOVA, post hoc Tukey’s multiple comparison test.