Powered by mitochondria’s adenosine triphosphate, neurons require this energy to spread across body distances. As adults age, mitochondria slows down due to neurons producing protein, syntaphilin, which stops the motion of mitochondria.
The Journal of Cell Biology published the study, “Facilitation of axon regeneration by enhancing mitochondrial transport and rescuing energy deficits.”
Here are five insights:
1. The researchers thought mitochondria’s slowdown may contribute to the inability of adult neurons to regenerate.
2. When a mouse axon became severed, the surrounding mitochondria were also damaged, researchers discovered. Thus, the mitochondria couldn’t produce adenosine triphosphate to help with neuron regeneration.
3. So, the researchers tried eliminating syntaphilin from the neurons, which allowed healthy mitochondria to replace the damaged mitochondria. The healthy mitochondria could then produce adenosine triphosphate, which aided neuron regeneration.
4. The study found mobilized mitochondria along neuronal axons played a part in mouse nerve cells repairing themselves following damage.
5. The researchers concluded neuron regeneration demands a combined approach of “mitochondrial transport and recovery of energy deficits.” The study authors noted their findings “may represent a valid therapeutic strategy to facilitate regeneration in the central and peripheral nervous systems after injury or disease.”
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