The failure of nerve cells to recover after injury and after some diseases is also related to loss of myelin, among other reasons. Meanwhile, the long axon thread of myelin enable high speed communication between neurons. In the absence of myelin, well coordination between the neurons may not be possible, resulting in below optimal function.
In a bid to restore myelin on restored axons, in a mouse model with optic nerve injury, scientists found a two-pronged approach. The work thus represents an important step in the functional restoration of cells in the central nervous system of adults.
New strategies leap over predecessor ones
In earlier research, several treatments discovered that could promote the restoration of injured axons in the optic nerve, but lack the ability to restore nerve function. The reason for this is restored axons are not myelinated. Meanwhile, in the new study published in Neuron, the researcher explains the reason why axons do not to remyelinate after injury.
In fact, in the adult brain, cells called oligodendrocytes precursors carry out myelination.
“And, for injured optic nerves, oligodendrocytes precursor cells fail to differentiate into mature myelination-competent oligodendrocytes,” found the researchers. This means they do not develop into cells capable of generating myelin and to function normal.
The research team discovered for reasons for this. Firstly, oligodendrocytes precursor cells in injured nerves release a protein known as GPR17, which obstructs the first step of differentiation of oligodendrocytes into mature cells. Secondly, inflammatory cells in injured nerves interfere with another step of differentiation of oligodendrocytes precursor cells.
The testing of a set of available compounds revealed that montelukast – an inflammatory used in the treatment of seasonal allergies and asthma – obstructed the development of GPR-17, discovered the first co-author of the study.