Small compounds mimicking the adhesion molecule L1 improve recovery in a zebrafish demyelination model

Demyelination, the loss of the myelin sheath around nerve fibers, leads to impaired nerve function and is associated with diseases like multiple sclerosis. This study investigates potential treatments to reduce demyelination and promote remyelination. The researchers used a zebrafish model of demyelination to test the effects of tacrine and duloxetine, two compounds that mimic the function of the L1 cell adhesion molecule, which is known to promote nerve regeneration. The results showed that both tacrine and duloxetine improved remyelination in the zebrafish, suggesting their potential as therapeutic agents for demyelinating diseases.

• 1
  Tacrine and duloxetine promote the regeneration of oligodendrocytes in the central nervous system after oligodendrocyte ablation in zebrafish.
• 2
  Both tacrine and duloxetine induce the regeneration of Schwann cells in the posterior lateral line after the ablation of Schwann cells.
• 3
  Tacrine, but not duloxetine, restores locomotor activity after demyelination in zebrafish larvae, suggesting a functional recovery.