Multiple sclerosis The phagocytes are overwhelmed in old age

A newly discovered cell type gives hope for better multiple sclerosis therapies

Scientists have apparently explored the reason why regeneration phases in patients with relapsing forms of multiple sclerosis are becoming less common as they get older. Relapsing multiple sclerosis causes acute illnesses that can cause nerve damage and disability. In the breaks between these attacks, the body has time to regenerate. As you get older, however, these breaks become shorter and the autoimmune affliction worsens continuously.

The research team led by Mikael Simons from the Max Planck Institute for Experimental Medicine in Göttingen showed that in mice with nerve lesions resembling multiple sclerosis, mice are less and less able to replace the damaged nerve cell myelin sheaths as they get older , Responsible for this process were the phagocytes, also called microglia and macrophages. These are responsible for the removal of residual products. With advancing age, the phagocytes had increasingly problems to "dispose of" the residual products of the damaged nerve cells. The results of this study were published in two publications in the journal "Science".

Overworked phagocytes slow down the regeneration of nerve cells in multiple sclerosis. This effect increases with age. (Image: ag visual / fotolia.com)

What happens in a multiple sclerosis attack??

In the chronic inflammatory disease of the central nervous system multiple sclerosis (MS), immune cells degrade fatty myelin sheaths of nerve cells. The myelin sheaths play a crucial role in the function of the central nervous system. Because the particularly high-fat membrane isolates the nerve fibers so that electrical signals can be forwarded quickly and efficiently. If this membrane is damaged, sufferers can suffer from deficits such as paralysis. After an MS attack, the reconstruction of intact myelin sheath begins and patients recover. But the regeneration capacity decreases with age.

The regeneration of myelin sheaths - a vicious circle?

The researchers were able to document that fat molecules from the myelin sheath can trigger chronic inflammation if they are no longer transported away fast enough. "Myelin has a very high proportion of cholesterol," explains Professor Simons in a press release from the Technical University of Munich. If myelin is destroyed, the released cholesterol must be removed from the tissue. For the evacuation are Fresszellen, also called microglia and macrophages, responsible. They would take the damaged myelin sheath into the cell, digest it and transport the indigestible remnants via transport molecules out of the cell. If too many fat molecules accumulate in a short time, crystal formations can occur. This can have devastating effects on the phagocytes, which, as a result of crystal formation, activate a so-called inflammasome, which in turn leads to more immune cells being attracted.

The regeneration decreases with age

The scientists were able to show in mice that the Fresszellen their task grew worse and worse with age. The older the mice were, the worse the removal of cholesterol and the stronger the inflammation. "If we treated the animals with a drug that promotes the removal of cholesterol, the inflammation went back and the myelin sheaths were regenerated," explains Mikael Simons. The scientists now want to investigate whether this mechanism is suitable for therapies of MS patients in order to accelerate regeneration.

Further findings of the study

The scientists also discovered a new cell type in the study. It is a special form of the so-called oligodendrocytes. These belong to the glial cells in the brain, which are responsible for the myelination. "We assume that the BCAS1-positive oligodendrocytes we discovered represent an intermediate stage in the development of these cells," says Mikael Simons. They are only detectable for a relatively short time when myelin is formed. While these cells are particularly strong in neonates, they largely disappear in adults. However, according to the scientists, they reappear when myelin sheaths are damaged and need to be rebuilt. "We hope the BCAS-1 positive cells can help us find new medicines to regenerate myelin," said Simon. (Vb)