Loss of myelin in nerve cell fibers — the hallmark of multiple sclerosis (MS) — leads to a shortage of mitochondria, a cell’s powerhouse, denying these damaged fibers the energy they need to work as intended, a new study shows.
Boosting the migration of mitochondria to affected nerve fibers, supplying them with needed energy, may help to protect nerves from degeneration and halt disease progression. Indeed, it may offer a new way of treating progressive MS.
The study “Enhanced axonal response of mitochondria to demyelination offers neuroprotection: implications for multiple sclerosis” was published in the journal Acta Neuropathologica.
MS is caused by the destruction of myelin, the fat-rich substance that wraps around and insulates nerve cell fibers (axons). Axons are projections of nerve cells that conduct the electric impulses that allow these cells to communicate.
To work as intended, damaged axons require large amounts of energy, which is provided by mitochondria. To compensate for the resulting energy imbalance, neurons respond by increasing their mitochondrial content. Mitochondria are small cellular organelles that work as the cell’s power plant: they produce energy molecules such as ATP, the most common cellular energy source.
However, in nerve cells of MS patients, mitochondria function is often affected. Evidence suggests people with progressive MS have genetic alterations that impair energy production.
A team led by researchers at the University of Edinburgh investigated whether targeting mitochondria in neurons could help mitigate the loss of myelin (demyelination). The study was supported by the National MS Society.
Researchers hypothesized that neurons would respond to demyelination by moving mitochondria from the neuron’s body to the damaged axon.
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