News

An international team reports that myelin damage results in a shortfall in the ability of axons (nerve cell fibers) to produce energy, and that targeting this process with treatment can protect axons from damage. This study identifies a new approach that may protect nerve cells from harm to stop or prevent MS progression.

• In MS, myelin, the fatty substance that surrounds and protects axons, is destroyed. This loss of myelin can affect the function and survival of nerve cells. Some research suggests that nerve cells may die due to damage to tiny energy-producing factories inside the cells, called mitochondria.
• In brain tissue obtained from people with MS via autopsy, and in mouse models, this team found that when myelin is damaged, the capacity of axons to produce energy is decreased. Mitochondria mobilize from the nerve cell body to the axon to compensate, but this process is not sufficient to offset the effects of myelin damage.
• When the team administered pioglitazone, a treatment that can increase mitochondrial growth, axonal structure and function was protected from damage. The authors comment that, to be effective, such a strategy would have to be combined with treatments that stop the immune attack and restore function.
• This research is partly funded by grants from the National MS Society, the MS Society of the United Kingdom, the NIH, and a Challenge Award from the International Progressive MS Alliance.

“Enhanced axonal response of mitochondria to demyelination offers neuroprotection: implications for multiple sclerosis” by Simon Licht‑Mayer and Don Mahad, MD, PhD, MRCP, at the University of Edinburgh and colleagues worldwide, was published on June 22, 2020, in Acta Neuropathologica.