mTOR Inhibition Alleviates Mitochondrial Disease in a Mouse Model of Leigh Syndrome
Copyright policy )mTOR Inhibition Alleviates Mitochondrial Disease in a Mouse Model of Leigh Syndrome
More from mTOR Leigh syndrome is a rare, untreatable, inherited neurodegenerative disease in children that is caused by functional disruption of mitochondria, the cell's energy-producing organelles. Johnson et al. (p. 1524 , published online 14 November; see Perspective by Vafai and Mootha ) show that rapamycin, a drug used clinically as an immunosuppressant and for treatment of certain cancers, delayed the onset and progression of neurological symptoms in a mouse model of Leigh syndrome and significantly extended survival of the animals. Rapamycin inhibits the so-called “mTOR” signaling pathway, which is currently under intense study because it plays a contributory role in many common diseases.
- Seattle Children's Hospital United States
- University of Mary United States
- University of Washington United States
- Seattle Children's United States
Mice, Knockout, Sirolimus, Electron Transport Complex I, Mitochondrial Diseases, TOR Serine-Threonine Kinases, Brain, Mechanistic Target of Rapamycin Complex 1, Mice, Mutant Strains, Mitochondria, Disease Models, Animal, Mice, Neuroprotective Agents, Multiprotein Complexes, Animals, Molecular Targeted Therapy, Leigh Disease, Glycolysis
Mice, Knockout, Sirolimus, Electron Transport Complex I, Mitochondrial Diseases, TOR Serine-Threonine Kinases, Brain, Mechanistic Target of Rapamycin Complex 1, Mice, Mutant Strains, Mitochondria, Disease Models, Animal, Mice, Neuroprotective Agents, Multiprotein Complexes, Animals, Molecular Targeted Therapy, Leigh Disease, Glycolysis
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