High PI3K-Akt-mTORC1 activity inhibits Schwann cell differentiation, while after onset of myelination, residual PI3K-Akt-mTORC1 activity promotes myelin growth.

Endogenous synthesis of fatty acids by oligodendrocytes is essential for development and repair in the central nervous system.

Oligodendrocytes with an enhanced ability to withstand cytotoxic stress display an increased capacity to remyelinate demyelination lesions of the CNS in the presence of an inflammatory environment.

Yap and Taz regulate proliferation and differentiation of Schwann cells, driving radial sorting, myelination and myelin maintenance of peripheral nerves.

The ORMDL proteins function to restrain the de novo sphingolipid biosynthetic pathway during myelination, when there is a high demand for sphingolipids to prevent excessive accumulation of metabolic intermediates.

Results of a zebrafish whole-animal chemical screen for compounds that can rescue ear and myelination defects in an adhesion GPCR (Adgrg6/Gpr126) mutant.

Uncoupling the immunological response and degenerative processes from possible repair demonstrates that remyelination prevents axonal loss after inflammatory demyelination.

A cell-cell contact between microglial SIRPα and CD47 on neighboring cells is a critical module for phase conversion of microglia in the brain white matter and controls demyelination.

Although central nervous system (CNS) regeneration has been considered to be controlled by CNS microenvironment, CNS injury causes leading to leakage of circulating factors into CNS, which promotes CNS regeneration.

mTORC1 and c-Jun are implicated in a possible mechanism causing myelin loss downstream of mitochondrial dysfunction in Schwann cells.