Mitochondrial Modulation by Dichloroacetate Reduces Toxicity of Aberrant Glial Cells and Gliosis in the SOD1G93A Rat Model of Amyotrophic Lateral Sclerosis
Author:
Funder
Comisión Sectorial de Investigación Científica
Publisher
Springer Science and Business Media LLC
Subject
Pharmacology (medical),Clinical Neurology,Pharmacology
Link
http://link.springer.com/article/10.1007/s13311-018-0659-7/fulltext.html
Reference51 articles.
1. Brown RH, Al-Chalabi A. Amyotrophic lateral sclerosis. N Engl J Med 2017;377:162–172.
2. Smith EF, Shaw PJ, De Vos KJ. The role of mitochondria in amyotrophic lateral sclerosis. Neurosci Lett2017. https://doi.org/10.1016/j.neulet.2017.06.052.
3. Dupuis L, Pradat P-F, Ludolph AC, Loeffler J-P. Energy metabolism in amyotrophic lateral sclerosis. Lancet Neurol 2011;10:75–82.
4. Cassina P, Cassina A, Pehar M, et al. Mitochondrial dysfunction in SOD1G93A-bearing astrocytes promotes motor neuron degeneration: prevention by mitochondrial-targeted antioxidants. J Neurosci 2008;28:4115–4122.
5. Miquel E, Cassina A, Martínez-Palma L, et al. Modulation of astrocytic mitochondrial function by dichloroacetate improves survival and motor performance in inherited amyotrophic lateral sclerosis. PLoS One 2012;7:1–9.
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