Multiple sclerosis is a chronic inflammatory disease of the central nervous system. The inflammation processes damage the myelin, the lipid-rich insulating layer around some nerve cells, creating demyelinated lesions. Cells with damaged or lacking myelin can’t function properly and all this can lead to neurodegeneration. To make things worse, in multiple sclerosis the body’s own capability to remyelinate the nerve cells is diminished, whereas in healthy individuals remyelination is normal and protects us against this unwelcome process.

It has been established that one of the reasons for demyelination is reduced capacity of oligodendrocytes to regulate myelin membrane growth. In the last ten years or so, scientists came to believe that cholesterol has an important role in oligodendrocyte function deterioration. Patients with multiple sclerosis have disturbed brain lipid metabolism with brain cholesterol levels being low, whereas blood cholesterol levels are in the normal range. With progression of the disease even the blood cholesterol levels elevate, but we have no definitive answer to the question whether this elevated cholesterol levels are a contribution to the disease, a consequence of the disease or a body’s attempt to counterbalance the metabolic disruption.

More than a decade ago, a group of German scientists showed on mice that dietary cholesterol can mitigate the range of demyelination by restoring the oligodendrocytes normal function.

The brain has to have enough cholesterol to renew damaged myelin and in the new study by the same German group it was shown that the decreased levels of brain cholesterol is a factor in the diminished remyelination capacity. Using mice they found out that dietary cholesterol enters the nervous system, speeds up the remyelination processes and above all it doesn’t negatively affect inflammation.

So why is there a lack of cholesterol in the affected brain? There seems to be a range of dysfunction: lack of certain enzymes, a disruption in the cholesterol transport between cells because of the lack of apolipoprotein E, brain-blood barrier disruptions and decrease of the blood cholesterol levels also probably contributes to the impairment of cholesterol homeostasis in the brain (Berghoff et al., 2017).