A study published in Journal of Cell Biology sheds new light on the processes by which cells in the peripheral nervous system (PNS) effect repair following injury, disease, inherited mutations, or age. In the PNS, Schwann cells, which provide the myelin sheath protecting axons, are also able to clear away damaged myelin and direct the regenerative process. This is not the case with the myelin-producing cells in the central nervous system, oligodendrocytes, and hence, the CNS has limited regenerative and repair capability. The new findings, by researchers from Spain and the UK, suggest that the cleanup of damaged myelin may involve 2 different processes, phagocytosis, preceded by autophagy, with myelin debris inside of Schwann cells being carried to lysosomes in a process the authors term “myelinophagy.” A clearer understanding of the workings of this mechanism is key to the development of better treatment of diseases of the PNS that result in myelin damage (demyelination).
The research focused on mouse sciatic nerves, a component of the PNS, and observed that within 4 to 7 days after injury, there was an abundance of autophagosomes—which deliver cargo to lysosomes for degradation—compared with uninjured nerves, and these autophagosomes contained myelin debris. Inhibiting autophagy led to a notable reduction in myelin breakdown. The authors state that their findings lend support to the hypothesis that modulating myelinophagy can prevent myelin breakdown in demyelinating diseases or improve nerve repair after PNS damage, but that further research is needed.
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Read a news story about the research findings here.