Mechanisms identified to restore myelin sheaths after injury or in multiple sclerosis – University of Mainz

photo/©: Mert Duman
Remyelinated axons (light gray circular structures) in spinal cord after experimental focal degradation of myelin sheaths (dark rings), simulating a lesion caused by multiple sclerosis

 
A research team led by neurobiologist Professor Claire Jacob has identified an important mechanism that can be used to control the restoration of myelin sheaths following traumatic injury and in degenerative diseases. With the insights gained, the researchers were able to regenerate damaged myelin sheaths in mice by treating them with the active substance theophylline, thereby restoring their nerve cell function. The groundbreaking findings are the result of research carried out at Johannes Gutenberg University Mainz (JGU) and the University of Fribourg in Switzerland.

Neurons are composed of axons, i.e., long fiber-like extensions that transmit signals to other cells. Many of them are surrounded by a myelin sheath, a thick fatty layer that protects them and helps to transfer stimuli rapidly. Without myelin, the functional capacity of neurons – and therefore of the whole nervous system – is limited and neurons can easily degenerate. Multiple sclerosis (MS) is one of the diseases associated with myelin sheath degradation. MS patients suffer successive episodes of demyelination resulting in a progressive loss of function of their nervous system. Remyelination of the axons can prevent this.

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