Can Your Brain Repair Itself?
Meet The Cells That Rebuild The Protective Insulation Around Nerve Fibres.
The Biology Behind Myelin
Neurons are best known for transmitting electrical signals. But they cannot do everything alone.
In the brain and spinal cord, specialised cells called oligodendrocytes produce myelin by wrapping sections of their membranes around neuronal axons. This creates a multilayered insulating sheath.
But how exactly does this sheath make neural communication faster?
Nerve impulses travel along axons as electrical signals called action potentials. These signals propagate because an electrical change at one point along the membrane stimulates the next region, generating a new action potential.
In myelinated axons, however, this process works differently.
Myelin acts as an insulator, allowing electrical current to travel rapidly towards small uncovered gaps between myelin segments, called nodes of Ranvier.
It is at these nodes that action potentials are regenerated, rather than continuously along the entire axonal membrane.
This mechanism, known as saltatory conduction, allows nerve impulses to travel faster and with less energy consumption.
But myelin is not indestructible.
Inflammation, injury and certain neurological diseases can damage or destroy it, interfering with the transmission of nerve impulses.
One well-known example is multiple sclerosis (MS), a disease in which immune-mediated processes damage myelin in the central nervous system.
So, can the nervous system replace the myelin it has lost?
The Cells That Repair Myelin
Throughout the adult central nervous system, there is a population of cells called oligodendrocyte precursor cells (OPCs).
These cells retain the ability to divide and develop into mature oligodendrocytes.
When myelin is damaged, OPCs can respond to signals from the surrounding tissue.
Some migrate towards the affected area, proliferate and differentiate into new oligodendrocytes.
These newly formed cells can then produce myelin around axons that have lost their protective coating.
This process is called remyelination.
It is one of the clearest examples of the adult central nervous system's capacity for cellular repair.
However, remyelination does not always restore the original myelin structure, and successful repair also depends on the survival and condition of the underlying axon.
Why Doesn't Repair Always Work?
If the brain contains cells capable of rebuilding myelin, why can diseases such as multiple sclerosis cause lasting neurological damage?
The answer lies partly in the complexity of the repair process.
OPCs must receive the appropriate signals, reach the damaged region and successfully mature into myelin-producing oligodendrocytes.
Several factors can interfere with these steps.
For example, persistent inflammation can create an environment that makes repair more difficult.
As the nervous system ages, OPCs may also become less efficient at responding to damage and differentiating into mature oligodendrocytes.
In some MS lesions, precursor cells are present but fail to complete the final stages of maturation.
And even when remyelination occurs, it cannot necessarily reverse damage to axons that have already degenerated.
This means that having cells capable of repairing tissue does not mean that every injury can be repaired.
Why Does This Discovery Matter?
Understanding remyelination could transform how scientists approach demyelinating diseases. Many current treatments for multiple sclerosis focus on modifying the immune response and reducing inflammatory disease activity.
But preventing further damage and repairing existing damage are two different challenges.
An effective remyelination therapy could potentially help preserve nerve fibres and restore some lost function.
Researchers are therefore exploring strategies that support the nervous system's natural repair mechanisms, rather than focusing exclusively on preventing injury.
The adult brain is not a completely static organ. Even after development, specialised cell populations continue to respond to changes in their environment, maintain neural tissue and, under certain circumstances, contribute to its repair.
Conclusions
The brain's ability to repair damaged myelin reveals something remarkable about the nervous system: even in adulthood, certain cells retain the capacity to respond to injury and contribute to tissue repair.
Yet remyelination also highlights the limits of this ability. Although oligodendrocyte precursor cells can generate new myelin-producing cells, the process may become less effective with ageing, persistent inflammation or severe tissue damage.
Understanding what enables these cells to repair myelin, and what prevents them from doing so, could open new possibilities for treating diseases such as multiple sclerosis.
Rather than simply protecting the nervous system
from further damage, future therapies might also help it recover
some of what has already been lost.
Source:
Franklin, R. J. M., & Ffrench-Constant, C. (2017). Regenerating CNS myelin: from mechanisms to experimental medicines. Nature Reviews Neuroscience, 18, 753–769.
Lubetzki, C., et al. (2020). Remyelination in multiple sclerosis: from basic science to clinical translation. The Lancet Neurology, 19, 678–688.
Franklin, R. J. M., Frisén, J., & Lyons, D. A. (2021). Revisiting remyelination: Towards a consensus on the regeneration of CNS myelin. Seminars in Cell & Developmental Biology, 116, 3–9.
Lubetzki, C., Sol-Foulon, N., & Desmazières, A. (2020). Nodes of Ranvier during development and repair in the CNS. Nature Reviews Neurology, 16, 426–439.
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