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Figure 7 | Molecular Neurodegeneration

Figure 7

From: Amyloid beta dimers/trimers potently induce cofilin-actin rods that are inhibited by maintaining cofilin-phosphorylation

Figure 7

Upstream regulators of cofilin phosphorylation impact the ability of Aβd/t to induce rods. Rod formation was quantified in (A) dissociated hippocampal neuronal cultures or (B) organotypic hippocampal slices that were uninfected (Con), infected with control adenovirus expressing GFP (GFP) or with adenoviruses expressing various upstream regulators of cofilin phosphorylation. All viruses co-expressed a fluorescent protein marker and only neurons expressing the marker were scored in the dissociated cultures. In slices, infection rates were approximately 70% (see Additional file 5) and rods per field were quantified (it was not possible in slices to count rods only within infected neurons). Neurons or slices were infected 24 h prior to treatment with Aβd/t (1X) and were fixed and analyzed for rod formation 48 h after Aβd/t addition. Treatments that enhance cofilin dephosphorylation (the active phosphatases SSH-1L WT and CIN WT) in the dissociated cultures enhance rod formation with or without Aβd/t treatment (* = significant difference from untreated or GFP controls at p = 0.05; # significantly different from Aβd/t treated controls, p = 0.05). Treatments that inhibit cofilin dephosphorylation (LIMK1 WT and the active LIMK1T508EE), inhibit rod formation in response to Aβd/t in both dissociated neuronal cultures and in slices (n = 3).

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