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Myelinating to the neuronal axon

Damage to myelin producing cells could trigger nervous system inflammation

A new study provides evidence for oligodendrocyte (myelin making cell) death as a key event in triggering inflammation in the central nervous system.

A new model of MS

In MS, the immune system launches an attack on myelin, the cause of which remains unclear. In this study from the University of Chicago and Northwestern University, researchers used a mouse model to investigate whether oligodendrocyte death could trigger the immune attack that occurs in MS.

In this study, approximately 30 weeks after recovering from oligodendrocyte loss, the mice went onto develop a secondary disease characterised by extensive myelin and nerve loss, mimicking aspects of progressive MS. This provides evidence oligodendrocyte death could act as a trigger to an immune response against myelin.

The researchers then went on to show it was possible to prevent this trigger despite the death of oligodendrocytes, with specially developed nanoparticles. Development of this nanoparticle technology could lead to a clinical trial in people with MS in the future.

Conflicting theories

Many researchers currently believe MS is caused by an event outside of the nervous system triggering an immune response in certain people. As a result, confused immune cells enter the brain and attack the myelin resulting in a range of debilitating symptoms. This is known as the outside-in hypothesis.

Dual impact study

However, this study provides evidence to suggest MS may begin from inside the central nervous system, with damage or abnormalities to myelin and myelin-making cells triggering immune attacks and inflammation. This is known as the inside-out hypothesis. This laboratory study demonstrates two promising findings.

  1. It provides early stage evidence damage inside the central nervous system causes an immune response which can be prevented using nanoparticle technology in mice.
  2. It provides an effective new mouse model which could be used for testing therapies designed to protect the nervous system in the future. This is encouraging as current models have a number of limitations.

Further research is now needed to understand the role of oligodendrocyte death in relation to the immune system attack on myelin, but targeting myelin repair is already a key strategy for many research groups within the field of MS. This research further illustrates the importance of finding therapies that can protect and repair myelin making cells as effective treatments for people with MS.

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