Key Takeaways

• Myelin is a white, fatty membrane of lipids and proteins that insulates axons.
• Oligodendrocytes myelinate the CNS; Schwann cells myelinate the PNS.
• Nodes of Ranvier enable saltatory conduction, dramatically speeding nerve impulses.
• Core myelin proteins — MBP, PLP1, MOG, MAG and CNPase — are the biomarkers used to track myelin integrity.
• Demyelination underlies multiple sclerosis, Guillain-Barré syndrome and the leukodystrophies.
• Remyelination is possible, but becomes inefficient with age and chronic inflammation.

Contents

• What is Myelin?
• Who Makes Myelin? Oligodendrocytes vs Schwann Cells
• Neuron Anatomy and the Role of Axons
• Nodes of Ranvier and Saltatory Conduction
• The Key Myelin Proteins
• Myelin Damage: Causes and Consequences
• Demyelination and Multiple Sclerosis
• Remyelination and Myelin Restoration
• Frequently Asked Questions

Myelin Marker ELISA Kits

These validated sandwich ELISA kits quantify the structural myelin proteins and axonal-damage markers used across demyelination and remyelination research.

Human MBP ELISA Kit

Myelin basic protein compacts the sheath and is the classic marker of active myelin breakdown in CSF and serum.

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Human PLP1 ELISA Kit

Proteolipid protein 1 is the single most abundant myelin protein, holding adjacent membrane wraps together.

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Human MOG ELISA Kit

Myelin oligodendrocyte glycoprotein sits on the outermost sheath surface and is the target antigen in MOGAD.

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Human MAG ELISA Kit

Myelin-associated glycoprotein mediates the axon–glia contact that maintains the sheath.

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Human CNPase ELISA Kit

CNPase is an oligodendrocyte-enriched enzyme widely used as a marker of myelinating capacity.

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Human NEFL ELISA Kit

Neurofilament light chain reports the axonal damage that follows sustained demyelination.

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What is Myelin?

Myelin is a specialised, tightly compacted extension of the glial cell membrane that spirals around the axon of a nerve cell to form an insulating sheath. Unlike most biological membranes, myelin is dominated by lipid: roughly 70 to 85 per cent of its dry weight is lipid, chiefly cholesterol, galactocerebroside and sphingomyelin, with the remaining fraction made up of a small number of highly abundant proteins. That unusual composition gives myelin both high electrical resistance and low capacitance, and it is also what makes it appear white — which is why myelin-rich regions of the brain and spinal cord are called white matter, in contrast to the cell-body-rich grey matter.

Functionally the sheath does three jobs at once. It insulates the axon so current is not lost across the membrane, it prevents electrical crosstalk between neighbouring fibres, and it provides metabolic support to the axon it wraps — oligodendrocytes shuttle lactate and pyruvate into the axon through monocarboxylate transporters, sustaining fibres far too long to be supplied by the neuronal cell body alone. Myelin is therefore not passive packaging; it is an active partner in neuronal survival, which is why demyelination is so often followed by axonal degeneration.

Who Makes Myelin? Oligodendrocytes vs Schwann Cells

Two entirely different glial cell types build myelin, one in each half of the nervous system. In the brain and spinal cord the job belongs to oligodendrocytes, which extend multiple processes and can myelinate up to 50 separate axon segments at once. In the peripheral nervous system Schwann cells do the work, but each wraps a single internode on a single axon. That difference matters clinically: one dying oligodendrocyte strips myelin from dozens of axons simultaneously, which is part of why CNS demyelinating disease is so disabling.

Neuron Anatomy and the Role of Axons

The axon is the long, cable-like projection that carries the action potential away from the neuron cell body toward the axon terminal, where neurotransmitter is released onto the next cell. Dendrites collect incoming signals at one end of the neuron, the cell body integrates them, and the axon transmits the result — sometimes over a metre, as in the motor neurons running from the spinal cord to the foot. Myelin wraps the axon in discrete segments called internodes.

Axon diameter, internode length and sheath thickness are tuned together, and all three influence conduction velocity. The ratio of axon diameter to total fibre diameter — the g-ratio — sits near 0.6 to 0.7 in healthy CNS white matter, and a rising g-ratio is a reliable sign that myelin is thinning.

Nodes of Ranvier and Saltatory Conduction

Myelin does not run continuously along the axon. Every millimetre or so it is interrupted by a short, bare gap of about one micrometre known as a Node of Ranvier. These nodes are densely packed with voltage-gated sodium channels, while the myelinated internodes between them have very few. The action potential therefore cannot regenerate under the sheath — current flows passively down the insulated internode and the impulse is regenerated only at the next node, appearing to leap from node to node. This is saltatory conduction, from the Latin saltare, to jump.

The payoff is enormous. An unmyelinated axon conducts at roughly 0.5 to 2 metres per second; a myelinated axon of the same diameter conducts at up to 120 metres per second — an increase of around 100-fold — while consuming far less ATP, because sodium influx is restricted to the nodes. Achieving the same speed without myelin would demand axons of impossible diameter, and the human brain would not fit inside the skull.

The Key Myelin Proteins

Only a handful of proteins make up the non-lipid fraction of myelin, and each has become an important research biomarker. Their concentrations in cerebrospinal fluid, serum or tissue lysate are used to gauge sheath integrity, oligodendrocyte health and the extent of underlying axonal injury.

Myelin Damage: Causes and Consequences

Myelin can be damaged in several distinct ways. Autoimmune attack is the best known — the immune system recognises myelin antigens such as MOG or MBP as foreign and mounts a T-cell and antibody response against them. But myelin is also lost to direct physical injury of the brain or spinal cord, to viral and bacterial infection, to chronic hypoxia and small-vessel disease, to toxins and heavy metals, to vitamin B12 deficiency, and to inherited defects in the genes encoding myelin proteins or the enzymes that build myelin lipids.

Whatever the cause, the consequence at the axon is the same. Stripped of insulation, current leaks across the membrane, conduction slows, and eventually the action potential fails to propagate at all — a conduction block. Patients experience this as numbness, tingling, weakness, blurred or double vision, poor coordination and profound fatigue. Sustained demyelination then leaves the axon metabolically unsupported and vulnerable, and axonal transection follows. That secondary axon loss, tracked in the clinic by rising neurofilament light levels, is what converts a relapsing disease into a progressive one.

Activated microglia sit at the centre of this process. They clear myelin debris — a necessary step before repair can begin — but they also release TNF-alpha, IL-1 beta, nitric oxide and reactive oxygen species that injure oligodendrocytes and drive them into apoptosis, creating a self-sustaining cycle of inflammation and demyelination.

Demyelination and Multiple Sclerosis

Multiple sclerosis is the archetypal demyelinating disease, affecting an estimated 2.8 million people worldwide and typically presenting between the ages of 20 and 40, with women affected two to three times as often as men. Autoreactive T cells cross the blood-brain barrier, recognise myelin antigens, and recruit B cells and macrophages that strip the sheath and destroy the oligodendrocytes that made it. The resulting focal lesions — plaques — are scattered through the optic nerves, brainstem, cerebellum, periventricular white matter and spinal cord, and it is this dissemination in space and time that gives the disease its name.

MS is not the only demyelinating disorder. Neuromyelitis optica targets aquaporin-4 on astrocytes; MOG antibody-associated disease targets myelin oligodendrocyte glycoprotein directly; Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy strip peripheral myelin; and the leukodystrophies are inherited failures of myelin synthesis or maintenance. Distinguishing them increasingly depends on antigen-specific antibody testing alongside imaging.

Remyelination and Myelin Restoration

The adult CNS can repair myelin. Oligodendrocyte precursor cells, which make up roughly five per cent of all cells in the adult brain, are recruited to the lesion, proliferate, differentiate into mature oligodendrocytes and lay down new sheaths. Remyelinated segments are thinner and shorter than the originals — visible as so-called shadow plaques — but they restore conduction and, critically, restore the metabolic support that keeps the axon alive.

The problem is that remyelination becomes progressively less efficient with age and with repeated attacks. Precursor cells are still present in chronic lesions but fail to differentiate, blocked by inhibitory signals in the lesion environment including myelin debris itself, hyaluronan and MAG. This is why so much therapeutic effort now targets the differentiation step rather than the immune attack, and why efficient debris clearance — a microglial function — is seen as a prerequisite for successful repair. Adequate vitamin B12 and vitamin D, exercise and control of inflammation all support the process, though no approved remyelinating drug yet exists.