Scientists from Catherine Lubetzki and Bruno Stankoff's team at Paris Brain Institute have developed a new tool to test the potential of molecules in repairing myelin sheath lesions in multiple sclerosis (MS) patients. The team used genetically modified Xenopus tadpoles to count the number of myelin-producing oligodendrocytes in the optic nerve and correlate it with the animals' motor and behavioral abilities. The study was published in the journal Brain.

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After exposing the tadpoles to metronidazole, a substance inducing oligodendrocyte loss and impaired visual abilities, the team observed spontaneous myelin repair measured by an increase in the total number of oligodendrocytes and improvement in visual test results. Then, they showed that this phenomenon could be accelerated by presenting tadpoles with molecules that promote remyelination.

Despite considerable therapeutic advances in controlling the inflammatory component of MS, there is still a progression of disability in patients due to neurodegeneration. Remyelination, the process of repairing myelin sheath lesions, is challenging. One reason for these failures is that, in most cases, during preclinical testing, efficacy was evaluated on histology only, while functional recovery had not been assessed.

This new tool could potentially help bridge the link between visual disorders and associated demyelination lesions. By monitoring in vivo, researchers can test new drugs' remyelination potential before launching long and costly clinical trials. There is an urgent need to find molecules capable of acting on demyelination, which, in its chronic form, leads to irreversible axon damage responsible for neuronal death.