| Literature DB >> 26964504 |
David Kremer1, Peter Göttle1, Hans-Peter Hartung2, Patrick Küry3.
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 saltatory conduction and thus accelerated information processing. However, a number of CNS diseases harm or destroy myelin and oligodendrocytes (myelin-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 remyelination 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.Entities:
Keywords: myelin repair; neuroregeneration; oligodendroglial cells; therapies; white matter
Mesh:
Year: 2016 PMID: 26964504 DOI: 10.1016/j.tins.2016.02.004
Source DB: PubMed Journal: Trends Neurosci ISSN: 0166-2236 Impact factor: 13.837