MS (multiple sclerosis) is most prevalent in Northern Europe and Canada, and more common in the northernmost latitudes. In recent years, the number of cases has grown particularly among women.
The disease causes the patient’s own immune system to attack a protective coating known as myelin that surrounds nerve cells. When this sheath is destroyed, neuronal function decreases and the cells can ultimately die. This can result in visual disturbances, fatigue, mobility difficulties and other neurological symptoms that may be permanent.
No treatment for neural damage
Current MS drugs suppress the immune system’s overactivation, but are unable to repair the neural damage caused. This is a particular problem in the progressive form of the disease, where damage accumulates slowly over the years.
Researchers have long sought ways to initiate remyelination, a process where the destroyed myelin sheath grows back and the neurons recover. However, all drug candidates trialled so far have failed. The problem is that, particularly in the later stages of MS, the disease creates in the central nervous system local tissue conditions that inhibit remyelination.
Two solutions with the same outcome
In his doctoral thesis, Tapani Koppinen from
In the first approach, a drug molecule targets a stress mechanism intrinsic to brain cells. In areas damaged by MS, this stress response is constantly in overdrive, effectively preventing tissue-repairing cells from doing their job. When the mechanism was blocked using the new drug molecule, remyelination was significantly enhanced and accelerated in brain tissue with MS-like damage. The study was published in the
The second approach focuses on scar tissue formed around affected areas, which serves as a physical barrier to neural regeneration. By affecting the composition of this scar tissue with the second drug molecule, this approach also succeeded in promoting neuronal recovery. An article focusing on this approach was published in the
Surprisingly, these two drugs based on entirely different mechanisms led to very similar results: significant remyelination and reduced neuroinflammation in disease models, that is, animal and cell tests modelling the tissue pathology of MS.
First drug that boosts remyelination requires further research
For the time being, the results were achieved in laboratory animals and cell models. The more complex tissue conditions of human MS make it necessary to investigate the efficacy of the drug molecules in humans. One challenge for drugs targeting the brain is the blood-brain barrier, which blocks many substances from entering the brain. The researchers nevertheless demonstrated that both molecules effectively reach the central nervous system in laboratory animals.
“The goal is to enable the molecules we have developed to reach clinical trials, which could one day produce the first drugs that enhance remyelination in MS. In the meantime, our findings can help in investigating the pathogenic mechanisms of MS that inhibit remyelination,” Koppinen says.
Information about the doctoral thesis
Tapani Koppinen, MSc (Pharmacy), will defend his doctoral thesis entitled ‘Enhancing remyelination by overcoming extrinsic and intrinsic inhibitory factors’ on 8 May 2026 at 13.00 at the Faculty of Pharmacy, University of Helsinki. The public defence will take place at Biocenter 2, room 2041, Viikinkaari 5.
Professor Robin Franklin, FRS, from the University of Cambridge will serve as the opponent and Associate Professor Merja Voutilainen, the thesis supervisor, as the custos.
The thesis is also available in electronic form through the