Traumatic injuries to the brain, spinal cord, and optic nerve in the central nervous system (CNS) often result in catastrophic loss of sensory, motor, and visual functions.

Axons extending from neurons are responsible for transmitting signals between neurons and from the brain to the muscles and glands. The first step for successful axonal regeneration is the activation of a growth program that includes the formation of active growth cones and the synthesis and transport of materials for axon repair. All these processes require large amounts of energy and active transfer of mitochondria (the cell’s energy center) to the damaged axons at the far end.

Therefore, damaged neurons face particular challenges, requiring long-distance transport of mitochondria from the soma (cell body) to distal regenerating axons. The research team identified M1, a therapeutic small molecule that can enhance mitochondrial fusion and motility, resulting in sustained long-range axonal regeneration. Regenerated axons elicited neural activity in targeted brain regions and restored visual function within four to six weeks of optic nerve injury in M1-treated mice.

So far, these are the first results, the group will continue to investigate.

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Source: Ferra

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