Myelinogenesis

Myelinogenesis is generally the proliferation of myelin sheaths throughout the nervous system, and specifically the progressive myelination of nerve axon fibers in the central nervous system. This is a non-simultaneous process that occurs primarily postnatally in mammalian species, beginning in the embryo during the midst of early development and finishing after birth.

The myelination process allows neuronal signals to propagate down an axon more swiftly without the loss of signal. This enables better connectivity within specific brain regions and also improves broader neuronal pathways connecting spatially separate regions required for many sensory, cognitive, and motor functions.

Some scientists consider myelination to be a key human evolutionary advantage, enabling greater processing speeds that lead to further brain specialization. Myelination continues for at least another 10 to 12 years after birth before an individual is fully developed. While the rate at which individual children develop varies, the sequence of development is the same for all children (with a range of ages for specific developmental tasks to take place).

Oligodendrocytes are responsible for the creation of myelin sheaths. There are “two stages of OL markers, differentiation of OPCs to OLs, and ensheathment of axons…”.

Although the mechanisms and processes of myelination are yet to be fully understood, some specific stages in this process have become clear:

The principal molecular mechanisms that control the process and sequence of myelinogenesis are not entirely known. Numerous studies have primarily focused on simplifying the underlying neuronal control of myelinogenesis and such studies have provided several possibilities.

One early study focused on the signaling of oligodendrocyte myelination by regenerating peripheral axons. Researchers studied regenerating PNS axons for 28 weeks in order to investigate whether or not peripheral axons stimulate oligodendrocytes to begin myelination. Experimental induction of myelination by regenerating peripheral axons demonstrated that Schwann cells and oligodendrocytes have a shared mechanism to stimulate myelination. A similar study working to provide evidence for neuronal regulation of myelinogenesis suggested that myelin formation was due to Schwann cells that were controlled by an undefined property of an associated axon.

Another such study in mice determined that the helix-loop-helix transcription factor, OLIG1, plays an integral role in the process of oligodendrocyte myelinogenesis. OLIG1 controls regulation in several myelin related genes, while suppressing others. On a cellular level, the study experimentally demonstrated that OLIG1 is necessary in order to stimulate myelination by oligodendrocytes in the brain. However, spinal cord related oligodendrocytes demonstrated a significantly smaller need of OLIG1 regulation in order to begin myelination.

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