Madhu M. Kanchi, Muthu K. Shanmugam, Grishma Rane, Gautam Sethi, Alan P. Kumar, Drug Discovery Today, 2017, ISSN 1359-6446, doi:10.1016/j.drudis.2017.08.001.
Vitamin E family members: tocotrienols and tocopherols are widely known for their health benefits. Decades of research on tocotrienols have shown they have diverse biological activities such as antioxidant, anti-inflammatory, anticancer, neuroprotective and skin protection benefits, as well as improved cognition, bone health, longevity and reduction of cholesterol levels in plasma. Tocotrienols also modulate several intracellular molecular targets and, most importantly, have been shown to improve lipid profiles, reduce total cholesterol and reduce the volume of white matter lesions in human clinical trials. This review provides a comprehensive update on the little-known therapeutic potentials of tocotrienols, which tocopherols lack in a variety of inflammation-driven diseases.
Remarks: EPI-743, sin: alpha-tocotrienol quinone, vatiquinone or Vincerinone. BioElectron Technology Corporation (Edison Pharmaceutical)
Thursday, August 17, 2017
Targeting Mitochondrial Dysfunction in Neurodegenerative Disease
The Dana Foundation. By Kayt Sukel, August 15, 2017
It’s long been known that the brain is an energy glutton: Most estimates suggest that it requires about 20 percent of the body’s total energy stores to work effectively. That energy is produced by mitochondria, specialized rod-shaped organelles in every cell in the body. So perhaps it is no surprise that problems with mitochondrial function in neurons have been linked to a host of progressive neurodegenerative disorders—one of which is Friedreich’s ataxia, a rare but devastating disease that progressively kills off nerve cells in the brain and spinal cord. Now, scientists at the University of California, Davis have identified how frataxin, the gene that causes Friedreich’s ataxia, affects mitochondrial function. That understanding may lead to new, more effective potential treatments for Friedreich’s ataxia as well as other forms of neurodegenerative disease.
Cortopassi hopes to take dimethyl fumarate (DMF) to clinical trial for Friedreich’s ataxia patients soon. He also thinks measuring mitochondrial number could be an important biomarker to test the efficacy of treatments for other neurodegenerative disorders as well. Manfredi agrees.
It’s long been known that the brain is an energy glutton: Most estimates suggest that it requires about 20 percent of the body’s total energy stores to work effectively. That energy is produced by mitochondria, specialized rod-shaped organelles in every cell in the body. So perhaps it is no surprise that problems with mitochondrial function in neurons have been linked to a host of progressive neurodegenerative disorders—one of which is Friedreich’s ataxia, a rare but devastating disease that progressively kills off nerve cells in the brain and spinal cord. Now, scientists at the University of California, Davis have identified how frataxin, the gene that causes Friedreich’s ataxia, affects mitochondrial function. That understanding may lead to new, more effective potential treatments for Friedreich’s ataxia as well as other forms of neurodegenerative disease.
Cortopassi hopes to take dimethyl fumarate (DMF) to clinical trial for Friedreich’s ataxia patients soon. He also thinks measuring mitochondrial number could be an important biomarker to test the efficacy of treatments for other neurodegenerative disorders as well. Manfredi agrees.
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