2009
DOI: 10.1016/j.nbd.2009.06.011
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Y-27632 improves rotarod performance and reduces huntingtin levels in R6/2 mice

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Cited by 62 publications
(61 citation statements)
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References 38 publications
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“…Fasudil prevents dopaminergic neuron degeneration and improves motor performance in a mouse model of Parkinson disease through stimulation of the Akt-mediated neuroprotective pathway (Tonges et al, 2012). This neuroprotection also supports the beneficial effect of pharmacologic ROCK inhibition in the R6/2 HD mouse model of Huntington disease (Li et al, 2009). In the mouse model of amyotrophic lateral sclerosis (hSOD1 G93A ), neuron loss has been attributed to ROCKmediated inhibition of Akt signaling, and inhibition of this pathway by fasudil slows disease progression and prolongs survival time (Takata et al, 2013).…”
Section: B Clinical Evaluation and Potential Applications Of Rho-asssupporting
confidence: 54%
“…Fasudil prevents dopaminergic neuron degeneration and improves motor performance in a mouse model of Parkinson disease through stimulation of the Akt-mediated neuroprotective pathway (Tonges et al, 2012). This neuroprotection also supports the beneficial effect of pharmacologic ROCK inhibition in the R6/2 HD mouse model of Huntington disease (Li et al, 2009). In the mouse model of amyotrophic lateral sclerosis (hSOD1 G93A ), neuron loss has been attributed to ROCKmediated inhibition of Akt signaling, and inhibition of this pathway by fasudil slows disease progression and prolongs survival time (Takata et al, 2013).…”
Section: B Clinical Evaluation and Potential Applications Of Rho-asssupporting
confidence: 54%
“…We devised a treatment strategy in which weekly dosing resulted in the pulsed induction of the HSR without any apparent toxicity. Treatment of R6/2 mice with HSP990 resulted in improved brain weight, a 20% reduction in aggregate load in brain tissues, and a 30% improvement in rotarod performance, effects comparable to those mediated by other treatment strategies (39,(49)(50)(51). However, HSP990 did not restore all aspects of disease progression, as grip strength, body weight and hypoactivity remained unchanged.…”
Section: Discussionmentioning
confidence: 86%
“…Shao et al showed that profilin suppresses Htt-NTF aggregation through direct interactions with Htt-NTFs (51). Increased expression of profilin reduces intracellular aggregation of Htt-NTFs and diminishes the toxicity of Htt-NTFs in cell lines, primary neurons, model organisms, and transgenic mice (52). Therefore, a direct therapeutic approach to HD could involve the design of ligands that mimic the effects of profilin on Htt-NTF aggregation and alleviation of toxicity.…”
mentioning
confidence: 99%