Table 1.

Differences regarding myelination in CNS vs. PNS.

CNS	PNS
Myelin sheaths are formed by oligodendrocytes.	Myelin sheaths are formed by Schwann cells (the only glial cell type in peripheral nerves). The myelination of PNS axons by Schwann cells is characterized by the sequential appearance of three different types of nerve fibers: (fetal, promyelin, and myelinated nerve fibers).
Myelination appears when axonal diameter is >0.2 μm.	Myelination occurs only if axonal diameter is >0.7 μm.
A single oligodendrocyte myelinates portions of multiple adjacent axons.	Schwann cells myelinate only one segment of a single axon.
Oligodendrocytes lack plasticity.	Schwann cells have remarkable plasticity.
Glycoproteins are minor constituents of CNS myelin.	Glycoproteins constitute at least 60% of PNS myelin proteins.
Cholesterol required for myelin synthesis is produced by the oligodendrocytes.	Peripheral nerves are hypomyelinated if cholesterol biosynthesis is lacking in Schwann cells [50].
Remyelination requires recruitment and differentiation of progenitor cells into new oligodendrocytes.	Schwann cells can dedifferentiate and assume an immature cell phenotype similar in response to injury.
Limited capacity of regeneration of central axons.	Peripheral axons regrow spontaneously after injury in a permissive environment reflecting the intrinsic regenerative capacity of neurons [51].
Remyelination is regulated by axonal signals that differ for oligodendrocytes and Schwann cells [52,53].	Remyelination is regulated by axonal signals different from those for oligodendrocytes [52,53]. Schwann cells only express a myelinating phenotype when contacting large axons producing threshold levels of neuregulin-1 type III [54].
CNS remyelination can also be achieved by Schwann cells [55] or by immature CNS glia with pluripotent capacity [56].	PNS demyelination reflects Wallerian degeneration and subsequent regeneration [57].