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Günther R, Balck A, Koch JC, et al. Rho Kinase Inhibition with Fasudil in the SOD1. Front Pharmacol. 2017;8:17doi: 10.3389/fphar.2017.00017.
Günther, R., Balck, A., Koch, J. C., Nientiedt, T., Sereda, M., Bähr, M., Lingor, P., & Tönges, L. (2017). Rho Kinase Inhibition with Fasudil in the SOD1. Frontiers in pharmacology, 817. https://doi.org/10.3389/fphar.2017.00017
Günther, René, et al. "Rho Kinase Inhibition with Fasudil in the SOD1." Frontiers in pharmacology vol. 8 (2017): 17. doi: https://doi.org/10.3389/fphar.2017.00017
Günther R, Balck A, Koch JC, Nientiedt T, Sereda M, Bähr M, Lingor P, Tönges L. Rho Kinase Inhibition with Fasudil in the SOD1. Front Pharmacol. 2017 Jan 31;8:17. doi: 10.3389/fphar.2017.00017. eCollection 2017. PMID: 28197100; PMCID: PMC5281550.
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Front Pharmacol. 2017 Jan 31;8:17. doi: 10.3389/fphar.2017.00017. eCollection 2017.

Rho Kinase Inhibition with Fasudil in the SOD1.

Frontiers in pharmacology

René Günther, Alexander Balck, Jan C Koch, Tobias Nientiedt, Michael Sereda, Mathias Bähr, Paul Lingor, Lars Tönges

Affiliations

  1. Department of Neurology, University Medicine GöttingenGöttingen, Germany; Department of Neurology, Technische Universität DresdenDresden, Germany.
  2. Department of Neurology, University Medicine GöttingenGöttingen, Germany; Institute of Neurogenetics, University of LübeckLübeck, Germany.
  3. Department of Neurology, University Medicine Göttingen Göttingen, Germany.
  4. Department of Neurogenetics, Max-Planck-Institute of Experimental Medicine Göttingen, Germany.
  5. Department of Neurogenetics, Max-Planck-Institute of Experimental MedicineGöttingen, Germany; Department of Clinical NeurophysiologyGöttingen, Germany.
  6. Department of Neurology, University Medicine GöttingenGöttingen, Germany; Cluster of Excellence Nanoscale Microscopy and Molecular Physiology of the BrainGöttingen, Germany.
  7. Department of Neurology, University Medicine GöttingenGöttingen, Germany; Cluster of Excellence Nanoscale Microscopy and Molecular Physiology of the BrainGöttingen, Germany; Department of Neurology, St. Josef-Hospital, Ruhr University BochumBochum, Germany.

PMID: 28197100 PMCID: PMC5281550 DOI: 10.3389/fphar.2017.00017

Abstract

Despite an improved understanding of the genetic background and the pathomechanisms of amyotrophic lateral sclerosis (ALS) no novel disease-modifying therapies have been successfully implemented in clinical routine. Riluzole still remains the only clinically approved substance in human ALS treatment with limited efficacy. We have previously identified pharmacological rho kinase (ROCK) inhibitors as orally applicable substances in SOD1.G93A transgenic ALS mice (SOD1

Keywords: Fasudil; ROCK; SOD1; mouse model of ALS; neuroprotection

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