David Kremer, Peter Göttle, Hans-Peter Hartung, and Patrick Küry

Abstract: 

The evolutionary acquisition of myelin sheaths around large caliber axons in the central nervous system (CNS) represented a milestone in the development of vertebrate higher brain function. Myelin ensheathment of axons enabled salta-tory conduction and thus accelerated information processing. However, a number of CNS diseases harm or destroy myelin and oligodendrocytes (mye-lin-producing cells), ultimately resulting in demyelination. In the adult CNS, new oligodendrocytes can be generated from a quiescent pool of precursor cells, which – upon differentiation – can replace lost myelin sheaths. The efficiency of this spontaneous regeneration is limited, which leads to incomplete remyeli-nation and residual clinical symptoms. Here, we discuss CNS pathologies characterized by white matter degeneration and regeneration and highlight drugs that could potentially serve as remyelination therapies.