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fAβ induces neuronal dystrophy and increased phosphorylation of cofilin. A, Rat hippocampal cultures were treated at day 7 with vehicle (control) or 20 μm fibrillar Aβ1–40 (fAβ40) and fixed at day 8. Confocal images were taken of cultures stained with rhodamine–phalloidin (F-actin) and with antibodies to P-cofilin and to tubulin class III (tubulin). Note that fAβ-treated cultures exhibit an increased level in P-cofilin and altered distribution of F-actin and significant neuritic dystrophy. Scale bar, 20 μm. B, Hippocampal cultures were treated with vehicle (ct), 20 μm fibrillar Aβ1–40 (fAβ40), or 20 μm soluble Aβ1–40 (sAβ40) and harvested after 24 h. Cell lysates were analyzed in triplicate by Western blot with antibodies against P-cofilin and tubulin; densitometric determination showed a significant increase in the P-cofilin level after fAβ treatment (∗p < 0.016, <t>ANOVA</t> followed by <t>the</t> <t>LSD</t> post hoc test). Similar results were obtained in at least three independent experiments. C, Rat hippocampal cultures were treated with 20 μm fAβ25–35 (fAβ35) for the indicated period of time, and the levels of P-cofilin and tubulin were analyzed in triplicate samples by densitometry after Western blot with specific antibodies. A significant increase in the P-cofilin level was observed after fAβ at all time points analyzed (∗p < 0.005, ∗∗p < 0.001, ANOVA followed by the LSD post hoc test). Plots are shown in arbitrary desitometric units (ADU). Error bars indicate SEM.
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fAβ induces neuronal dystrophy and increased phosphorylation of cofilin. A, Rat hippocampal cultures were treated at day 7 with vehicle (control) or 20 μm fibrillar Aβ1–40 (fAβ40) and fixed at day 8. Confocal images were taken of cultures stained with rhodamine–phalloidin (F-actin) and with antibodies to P-cofilin and to tubulin class III (tubulin). Note that fAβ-treated cultures exhibit an increased level in P-cofilin and altered distribution of F-actin and significant neuritic dystrophy. Scale bar, 20 μm. B, Hippocampal cultures were treated with vehicle (ct), 20 μm fibrillar Aβ1–40 (fAβ40), or 20 μm soluble Aβ1–40 (sAβ40) and harvested after 24 h. Cell lysates were analyzed in triplicate by Western blot with antibodies against P-cofilin and tubulin; densitometric determination showed a significant increase in the P-cofilin level after fAβ treatment (∗p < 0.016, <t>ANOVA</t> followed by <t>the</t> <t>LSD</t> post hoc test). Similar results were obtained in at least three independent experiments. C, Rat hippocampal cultures were treated with 20 μm fAβ25–35 (fAβ35) for the indicated period of time, and the levels of P-cofilin and tubulin were analyzed in triplicate samples by densitometry after Western blot with specific antibodies. A significant increase in the P-cofilin level was observed after fAβ at all time points analyzed (∗p < 0.005, ∗∗p < 0.001, ANOVA followed by the LSD post hoc test). Plots are shown in arbitrary desitometric units (ADU). Error bars indicate SEM.
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fAβ induces neuronal dystrophy and increased phosphorylation of cofilin. A, Rat hippocampal cultures were treated at day 7 with vehicle (control) or 20 μm fibrillar Aβ1–40 (fAβ40) and fixed at day 8. Confocal images were taken of cultures stained with rhodamine–phalloidin (F-actin) and with antibodies to P-cofilin and to tubulin class III (tubulin). Note that fAβ-treated cultures exhibit an increased level in P-cofilin and altered distribution of F-actin and significant neuritic dystrophy. Scale bar, 20 μm. B, Hippocampal cultures were treated with vehicle (ct), 20 μm fibrillar Aβ1–40 (fAβ40), or 20 μm soluble Aβ1–40 (sAβ40) and harvested after 24 h. Cell lysates were analyzed in triplicate by Western blot with antibodies against P-cofilin and tubulin; densitometric determination showed a significant increase in the P-cofilin level after fAβ treatment (∗p < 0.016, <t>ANOVA</t> followed by <t>the</t> <t>LSD</t> post hoc test). Similar results were obtained in at least three independent experiments. C, Rat hippocampal cultures were treated with 20 μm fAβ25–35 (fAβ35) for the indicated period of time, and the levels of P-cofilin and tubulin were analyzed in triplicate samples by densitometry after Western blot with specific antibodies. A significant increase in the P-cofilin level was observed after fAβ at all time points analyzed (∗p < 0.005, ∗∗p < 0.001, ANOVA followed by the LSD post hoc test). Plots are shown in arbitrary desitometric units (ADU). Error bars indicate SEM.
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Image Search Results


fAβ induces neuronal dystrophy and increased phosphorylation of cofilin. A, Rat hippocampal cultures were treated at day 7 with vehicle (control) or 20 μm fibrillar Aβ1–40 (fAβ40) and fixed at day 8. Confocal images were taken of cultures stained with rhodamine–phalloidin (F-actin) and with antibodies to P-cofilin and to tubulin class III (tubulin). Note that fAβ-treated cultures exhibit an increased level in P-cofilin and altered distribution of F-actin and significant neuritic dystrophy. Scale bar, 20 μm. B, Hippocampal cultures were treated with vehicle (ct), 20 μm fibrillar Aβ1–40 (fAβ40), or 20 μm soluble Aβ1–40 (sAβ40) and harvested after 24 h. Cell lysates were analyzed in triplicate by Western blot with antibodies against P-cofilin and tubulin; densitometric determination showed a significant increase in the P-cofilin level after fAβ treatment (∗p < 0.016, ANOVA followed by the LSD post hoc test). Similar results were obtained in at least three independent experiments. C, Rat hippocampal cultures were treated with 20 μm fAβ25–35 (fAβ35) for the indicated period of time, and the levels of P-cofilin and tubulin were analyzed in triplicate samples by densitometry after Western blot with specific antibodies. A significant increase in the P-cofilin level was observed after fAβ at all time points analyzed (∗p < 0.005, ∗∗p < 0.001, ANOVA followed by the LSD post hoc test). Plots are shown in arbitrary desitometric units (ADU). Error bars indicate SEM.

Journal: The Journal of Neuroscience

Article Title: Phosphorylation of Actin-Depolymerizing Factor/Cofilin by LIM-Kinase Mediates Amyloid β-Induced Degeneration: A Potential Mechanism of Neuronal Dystrophy in Alzheimer's Disease

doi: 10.1523/JNEUROSCI.5567-05.2006

Figure Lengend Snippet: fAβ induces neuronal dystrophy and increased phosphorylation of cofilin. A, Rat hippocampal cultures were treated at day 7 with vehicle (control) or 20 μm fibrillar Aβ1–40 (fAβ40) and fixed at day 8. Confocal images were taken of cultures stained with rhodamine–phalloidin (F-actin) and with antibodies to P-cofilin and to tubulin class III (tubulin). Note that fAβ-treated cultures exhibit an increased level in P-cofilin and altered distribution of F-actin and significant neuritic dystrophy. Scale bar, 20 μm. B, Hippocampal cultures were treated with vehicle (ct), 20 μm fibrillar Aβ1–40 (fAβ40), or 20 μm soluble Aβ1–40 (sAβ40) and harvested after 24 h. Cell lysates were analyzed in triplicate by Western blot with antibodies against P-cofilin and tubulin; densitometric determination showed a significant increase in the P-cofilin level after fAβ treatment (∗p < 0.016, ANOVA followed by the LSD post hoc test). Similar results were obtained in at least three independent experiments. C, Rat hippocampal cultures were treated with 20 μm fAβ25–35 (fAβ35) for the indicated period of time, and the levels of P-cofilin and tubulin were analyzed in triplicate samples by densitometry after Western blot with specific antibodies. A significant increase in the P-cofilin level was observed after fAβ at all time points analyzed (∗p < 0.005, ∗∗p < 0.001, ANOVA followed by the LSD post hoc test). Plots are shown in arbitrary desitometric units (ADU). Error bars indicate SEM.

Article Snippet: B , The length of MAP2-positive dendrites was determined in 80 neurons from triplicate samples using MetaMorph software; statistical comparisons were made by ANOVA and the LSD post hoc test.

Techniques: Phospho-proteomics, Control, Staining, Western Blot

S3 peptide counteracts fAβ-induced dendritic retraction. Rat hippocampal cultures were treated for 24 h with vehicle (control) or 20 μm fAβ1–40 (fAβ40), with or without 7.5 μg/ml S3 peptide, and fixed and immunolabeled with anti-MAP2 antibody. A, Fluorescent images were taken at 40× magnification. Note that S3 peptide prevents the reduction in dendritic length induced by fAβ. Scale bar, 20 μm. B, The length of MAP2-positive dendrites was determined in 80 neurons from triplicate samples using MetaMorph software; statistical comparisons were made by ANOVA and the LSD post hoc test. ∗p < 0.0001, fAβ versus control and S3 peptide-treated cultures. Error bars indicate SEM. C, Western blot analysis showing the levels of P-cofilin and tubulin after 24 h of treatment with the indicated concentrations of fAβ1–40 and S3 peptide; samples are shown by duplicate.

Journal: The Journal of Neuroscience

Article Title: Phosphorylation of Actin-Depolymerizing Factor/Cofilin by LIM-Kinase Mediates Amyloid β-Induced Degeneration: A Potential Mechanism of Neuronal Dystrophy in Alzheimer's Disease

doi: 10.1523/JNEUROSCI.5567-05.2006

Figure Lengend Snippet: S3 peptide counteracts fAβ-induced dendritic retraction. Rat hippocampal cultures were treated for 24 h with vehicle (control) or 20 μm fAβ1–40 (fAβ40), with or without 7.5 μg/ml S3 peptide, and fixed and immunolabeled with anti-MAP2 antibody. A, Fluorescent images were taken at 40× magnification. Note that S3 peptide prevents the reduction in dendritic length induced by fAβ. Scale bar, 20 μm. B, The length of MAP2-positive dendrites was determined in 80 neurons from triplicate samples using MetaMorph software; statistical comparisons were made by ANOVA and the LSD post hoc test. ∗p < 0.0001, fAβ versus control and S3 peptide-treated cultures. Error bars indicate SEM. C, Western blot analysis showing the levels of P-cofilin and tubulin after 24 h of treatment with the indicated concentrations of fAβ1–40 and S3 peptide; samples are shown by duplicate.

Article Snippet: B , The length of MAP2-positive dendrites was determined in 80 neurons from triplicate samples using MetaMorph software; statistical comparisons were made by ANOVA and the LSD post hoc test.

Techniques: Control, Immunolabeling, Software, Western Blot

LIMK1 and fAβ-induced neuronal death. Rat hippocampal cultures were treated with vehicle (control) or 20 μm fAβ1–40 (fAβ40), with or without 7.5 μg/ml S3 peptide, and the number of viable neurons was scored. A, In nontransfected cultures, the effect of fAβ1–40 and S3 peptide on neuronal viability was assessed 24 h after treatment by Hoechst staining. B, C, In cultures that were cotransfected with GFP and either wt-LIMK1 (B) or kd-LIMK1 (C), neuronal viability was assessed 18 h after treatment by scoring GFP-expressing neurons. A, Representative experiment showing the effect of fAβ and S3 peptide in neuronal viability. More than 900 neurons were scored, and similar results were found in three independent experiments. Statistical comparisons were made by ANOVA (F(3,36) = 23.32) and the LSD post hoc test. ∗p < 0.001, fAβ versus control, S3 peptide, and fAβ+S3peptide. B, Effect of fAβ and S3 peptide on neuronal viability in GFP/wt-LIMK1-cotransfected neurons. A representative experiment is shown, >170 neurons were scored, and similar results were found in three independent experiments. Statistical comparisons were made by ANOVA (F(3,12) = 4.1464) and the LSD post hoc test. ∗p < 0.01, fAβ versus control, S3 peptide, and fAβ+S3peptide. Note that toxicity of fAβ is blocked by S3 peptide in nontransfected neuronal cultures that express endogenous levels of LIMK1 and in cultures that were transfected with wt-LIMK1. C, Effect of fAβ and S3 peptide on neuronal viability in GFP/kd-LIMK1-cotransfected culture. A representative experiment is shown, >110 neurons were scored, and similar results were found in three independent experiments. No significant effect of fAβ in neuronal viability was observed; statistical comparisons were made by ANOVA (F(3,12) = 0.69154; p = NS). Note that kd-LIMK transfection inhibits fAβ-induced neuronal death. Error bars indicate SEM.

Journal: The Journal of Neuroscience

Article Title: Phosphorylation of Actin-Depolymerizing Factor/Cofilin by LIM-Kinase Mediates Amyloid β-Induced Degeneration: A Potential Mechanism of Neuronal Dystrophy in Alzheimer's Disease

doi: 10.1523/JNEUROSCI.5567-05.2006

Figure Lengend Snippet: LIMK1 and fAβ-induced neuronal death. Rat hippocampal cultures were treated with vehicle (control) or 20 μm fAβ1–40 (fAβ40), with or without 7.5 μg/ml S3 peptide, and the number of viable neurons was scored. A, In nontransfected cultures, the effect of fAβ1–40 and S3 peptide on neuronal viability was assessed 24 h after treatment by Hoechst staining. B, C, In cultures that were cotransfected with GFP and either wt-LIMK1 (B) or kd-LIMK1 (C), neuronal viability was assessed 18 h after treatment by scoring GFP-expressing neurons. A, Representative experiment showing the effect of fAβ and S3 peptide in neuronal viability. More than 900 neurons were scored, and similar results were found in three independent experiments. Statistical comparisons were made by ANOVA (F(3,36) = 23.32) and the LSD post hoc test. ∗p < 0.001, fAβ versus control, S3 peptide, and fAβ+S3peptide. B, Effect of fAβ and S3 peptide on neuronal viability in GFP/wt-LIMK1-cotransfected neurons. A representative experiment is shown, >170 neurons were scored, and similar results were found in three independent experiments. Statistical comparisons were made by ANOVA (F(3,12) = 4.1464) and the LSD post hoc test. ∗p < 0.01, fAβ versus control, S3 peptide, and fAβ+S3peptide. Note that toxicity of fAβ is blocked by S3 peptide in nontransfected neuronal cultures that express endogenous levels of LIMK1 and in cultures that were transfected with wt-LIMK1. C, Effect of fAβ and S3 peptide on neuronal viability in GFP/kd-LIMK1-cotransfected culture. A representative experiment is shown, >110 neurons were scored, and similar results were found in three independent experiments. No significant effect of fAβ in neuronal viability was observed; statistical comparisons were made by ANOVA (F(3,12) = 0.69154; p = NS). Note that kd-LIMK transfection inhibits fAβ-induced neuronal death. Error bars indicate SEM.

Article Snippet: B , The length of MAP2-positive dendrites was determined in 80 neurons from triplicate samples using MetaMorph software; statistical comparisons were made by ANOVA and the LSD post hoc test.

Techniques: Control, Staining, Expressing, Transfection

Recurrence rates for acute treatments for migraine

Journal: The Journal of Headache and Pain

Article Title: Variability in recurrence rates with acute treatments for migraine: why recurrence is not an appropriate outcome measure

doi: 10.1186/s10194-022-01519-4

Figure Lengend Snippet: Recurrence rates for acute treatments for migraine

Article Snippet: We also included an unpublished post hoc analysis of MAP0004 (LEVADEX/SEMPRANATM, MAP Pharmaceuticals Inc., Irvine, CA), an orally inhaled formulation of dihydroergotamine (DHE) mesylate that was evaluated in clinical trials [ ].

Techniques: Medications