PNAS, 2017 · DOI: 10.1073/pnas.1714183114 · Published: October 24, 2017
The research investigates whether thin myelin sheaths, a sign of remyelination, persist over long periods and continue to support nerve function. The study uses two animal models: dogs with a genetic myelin disorder and cats with demyelination caused by irradiated food. In dogs with a genetic disorder causing delayed myelination, thin myelin sheaths were observed to persist for 13 years without harming the axons. Similarly, in cats with demyelination, thin remyelinated axons persisted for over two years. The findings suggest that thin myelin sheaths can endure for extended periods and maintain nerve function, which is crucial for developing effective strategies to promote myelin repair in conditions like multiple sclerosis.
Future strategies for promoting myelin repair should focus on the persistence of thin myelin sheaths as a marker of repair.
Thin myelin sheaths can support long-term axon integrity and function, reducing the need for strategies to restore myelin to normal thickness.
Remyelination is a robust endogenous form of repair in the CNS and a major therapeutic target in demyelinating diseases.