Cholesterol, although viewed in a negative light at some point, has proven of extreme importance in our electrochemical stimulation process. The aftereffect of myelin sheath regeneration are numerous, but crucially, the major component of regeneration (cholesterol) has to be recycled or made anew. Scientists led by Gesine Saher discovered that in chronic damages, recycling of cholesterol is nearly impossible leaving the production of brand new cholesterol as the only option. The nerve cells aid the assisting glia in the de novo synthesis of cholesterol for myelin sheath regeneration. This is another big step in the health sector, providing immeasurable hope for myelin disorders like multiple sclerosis.
What was done in the study?
When a nerve gets damaged, the first part to be affected is the cholesterol and lipid layer. This leaves the myelin with no insulator, and likewise the nerve with no myelin. In this acute phase, phagocytes in the brain collect cholesterol from defective myelin, reprocess it, and send it to the cells forming the new myelin. This process gets slow and complicated as the patient ages and is almost impossible when the disorder lasts longer and becomes chronic. This is because as time passes the phagocytes, which are very necessary for the process, develop into foam cells that are not needed in the recycling cycle. To top it, in chronic situations the frequent degeneration process leads to a permanent state of “naked” for affected nerve cells. Gesine Saher, however, believes that in this exact situation, the production of cholesterol from other sources begins.
Knowing the body strongly defends itself against itself, the team went full-board on extensive research on the body’s counter-attack on the destruction of cholesterol and lipids in the nervous system. The results of the research rested on the fact that in carrying it the normal body processes, the body subconsciously repairs the cholesterol issue with chronic myelin disorders. They used Pharmacological myelin-defective mouse models. They noticed the neurons supply the outrageous demand of cholesterol by small synthesis, and taking in lipid-rich lipoprotein. The climax of this research was the finding, that in the acute degeneration, the cholesterol production was on a decline; but the total reverse happens in the chronic state.
To clearly understand this implication, the team disabled the gene factor of neurons and myelin-forming cells in cholesterol synthesis. The result shows very minimal progress in regeneration of myelin sheaths; but in neurons and myelin-producing cells without this inactivity, the progress of regeneration for myelin sheaths was on an uptrend. They treated these mice with a cholesterol-enriching diet and observe positive performance in myelin regeneration.
Clinically, this team is developing a clinical therapy approach for patients with myelin disorders. This approach is to address acute and chronic situations simultaneously, although they have different repair mechanisms.
As usual, every new finding paves way for another finding and also makes medical diagnostics more accurate. However, the clinical challenge for this topic would be a skyrocket if successfully achieved. It would address many myelin disorders and neurodegenerative disorders.