Akt overexpression rescues Aβ42-induced toxicity without affecting levels of intraneuronal Aβ. Akt overexpression rescues Aβ42-induced toxicity without.

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Akt overexpression rescues Aβ42-induced toxicity without affecting levels of intraneuronal Aβ. Akt overexpression rescues Aβ42-induced toxicity without affecting levels of intraneuronal Aβ. A, Cortical neurons were infected with AdTet-On and AdTRE-Aβ42. Transgene expression was induced by 1 μg/ml Dox for 24 h (+, bottom), and cells were coinfected with Ad-LacZ, Ad-myrAkt (constitutively active Akt), or Ad-dnAkt (inactive Akt) as indicated. Ad-myrAkt fully protected against Aβ42-induced neuronal death, as measured by TUNEL staining (*p < 0.005). Coinfection with Ad-dnAkt or Ad-LacZ control did not affect Aβ42 toxicity. Values from three independent experiments are shown. Immunoblot analysis of Akt overexpression in primary neurons (right). B, Immunofluorescent images from primary neurons infected with AdTet-On and AdTRE-Aβ42. Cells were coinfected with Ad-GFP or Ad-myrAkt, as indicated. No apparent changes in levels or localization of Aβ were observed. C, Quantification of Aβ immunofluorescence from neurons with or without coexpression of GFP control or myrAkt. Ratio of Aβ42 intensity in processes divided by that in cell bodies was calculated, with the ratio standardized to 1.0 for cells without GFP or myrAkt coexpression. Error bars represent 1 SE. Results from three independent experiments are shown. n.s., Nonsignificant. Jordi Magrané et al. J. Neurosci. 2005;25:10960-10969 ©2005 by Society for Neuroscience