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Mitochondria May Play a Role in MS Development and Progression




















Recent attention to the role of mitochondria in the etiology of multiple sclerosis (what causes the disease) suggests that mitochondrial defects and mitochondrial structural and functional changes may contribute to the disease. Researchers studying mitochondria in multiple sclerosis believe abnormalities in mitochondrial dynamics impact cellular pathways such as inflammation and demyelination, ultimately impacting patients with multiple sclerosis.

Dr. Peizhong Mao and Dr. P. Hemachandra Reddy, of the Neurogenetics Laboratory at Oregon Health & Science University, identified five key abnormalities in the mitochondria that are involved in disease development and progression. Mitochondrial DNA defects, abnormal mitochondrial gene expression, defective mitochondrial enzyme activities, deficient mitochondrial DNA repair activity, and mitochondrial dysfunction have been shown to play a role, according the two researchers’ article, “Is Multiple Sclerosis a Mitochondrial Disease?” that was published in Biochimica et Biophysica Acta (BBA) – Molecular Basis of Disease.

“Neurons are highly dependent on oxidative energy metabolism,” wrote Dr. Mao and Dr. Reddy. “Deficient mitochondrial metabolism may generate more reactive oxygen species (ROS) that can wreak havoc in the cell.” A recent study published in Neurology, entitled “Mitochondrial DNA Sequence Variation in Multiple Sclerosis,” demonstrated that certain mitochondrial genetic variants are associated with multiple sclerosis. For example, patients with haplogroup J variants were at a 1.5-times increased risk for developing primary progressive multiple sclerosis.

Another look into mitochondrial involvement in multiple sclerosis was conducted by Dr. Lukas Haider at the Medical University of Vienna. “Recent data indicate that mitochondrial injury and subsequent energy failure are key factors in the induction of demyelination and neurodegeneration,” wrote Dr. Haider in the article, “Inflammation, Iron, Energy Failure, and Oxidative Stress in the Pathogenesis of Multiple Sclerosis,” which was published in Oxidative Medicine and Cellular Longevity. Since the brain accounts for such a large proportion of oxygen consumption in the mitochondria, cells in the brain are especially susceptible to oxidative stress, leading to the previously identified genetic variants as a result of damage. Without properly functioning mitochondria, cells within the brain cannot thrive.

Dr. Mao and Dr. Reddy discussed a few therapeutic approaches to treat multiple sclerosis by targeting the mitochondria. These therapies are considered more neuroprotective than immunomodulatory and are different from current treatments for multiple sclerosis. Inhibitors of proteins that allow oxidative stress to damage the mitochondria, such as intravenous mitoxantrone, might delay the progression of multiple sclerosis in relapsing-remitting or secondary progressive multiple sclerosis.

Enhancing mitochondrial DNA repair by targeting repair proteins to the mitochondria may also prove to be an effective means for treating multiple sclerosis, while also addressing the direct problem of mitochondrial dysfunction in the disease. At present, mitochondria-targeted antioxidants such as MitoQ can help address oxidative stress in the development of diseases such as Multiple Sclerosis by decreasing mitochondrial oxidative damage. Ubiquinone, the active ingredient in MitoQ, is identical to Coenzyme Q10, a well-known antioxidant. Some researchers believe that therapies such as these offer a novel approach to addressing the underlying cause of MS, and patients have reported it success in improving symptoms and quality of life as an alternative the currently FDA-approved multiple sclerosis therapies.

Story Source: The above story is based on materials provided by MULTIPLESCLEROSISNEWSTODAY
Note: Materials may be edited for content and length


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