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HOPE for FATIGUE

Could Mitochondrial Dysfunction Play a Role in the Onset of Multiple Sclerosis?

Recent advances in multiple sclerosis (MS) research point to abnormalities in mitochondrial function as a key factor in the onset and development of the disease. Dr. Lukas Haider at the Medical University of Vienna suggests that dysfunction of the mitochondria could impact the cellular pathways causing the inflammation and demyelination known to be the hallmark of this disease.

Researchers at the Neurogenetics Laboratory at Oregon Health & Science University, have identified five key abnormalities in the mitochondria that are involved in disease development and progression:

  1. Mitochondrial DNA defects
  2. Abnormal mitochondrial gene expression
  3. Defective mitochondrial enzyme activities
  4. Deficient mitochondrial DNA repair activity
  5. Mitochondrial dysfunction

Because the brain accounts for such a large percentage of oxygen consumption, cells in the brain are especially susceptible to oxidative stress, leading to the development of multiple sclerosis as a result of this damage. Without properly functioning mitochondria, cells within the brain are stressed and can malfunction.

Instead of only relying upon current immunomodulatory therapies for the treatment for MS, new approaches targeting the mitochondria are being explored to help provide optimal neuroprotection.  

The American Academy of Neurology has also reported that women with multiple sclerosis may have lower levels of important antioxidant and anti-inflammatory nutrients than healthy people. Mitochondrial support antioxidants are recommended to reduce oxidative stress and the risk of subsequent mitochondrial damage.

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