By Tim Newman
Multiple sclerosis (MS) is an autoimmune disease affecting more than 2.3 million people around the world. The condition attacks myelin, or the waxy coat around nerves, and compromises the nerves’ ability to transmit messages.
Over time, as the nerves’ function is steadily reduced, a range of symptoms – including problems with vision, muscle weakness, difficulty walking, and issues with balance and coordination – develop.
Current treatment focuses on preventing the immune system from causing further damage, and as it stands, no drugs can repair the damaged myelin.
Discovering a medication capable of rebuilding the damaged myelin would be a huge step forward. And according to the latest study, this may be just around the corner.
New MS drug on the horizon?
In 2014, studies carried out by Prof. Jonah R. Chan at the University of California, San Francisco showed that clemastine fumarate may be a candidate for the treatment of MS.
Because of the potential importance of the findings, the drug quickly progressed to clinical trials. This week, the results from a phase II clinical trial on clemastine fumarate are published in The Lancet.
Clemastine fumarate was first approved by the Food and Drug Administration (FDA) in 1977. It is an antihistamine medication for allergies and has been available over the counter since 1993. Its potential to treat MS is therefore as surprising as it is welcome.
According to principal investigator Dr. Ari Green, “To the best of our knowledge, this is the first time a therapy has been able to reverse deficits caused by MS. It’s not a cure, but it’s a first step toward restoring brain function to the millions who are affected by this chronic, debilitating disease.”
Clemastine fumarate on trial
The team studied the effects of clemastine fumarate on 50 individuals with long-standing MS over a 5-month period. Because the visual system is often one of the first to be affected, the researchers measured so-called visual evoked potentials (VEPs). This is a well-established method of assessing how quickly nerves conduct messages.
VEPs were measured by showing participants flickering patterns on a screen. Electrodes placed over the visual areas of the brain detected how long it took signals to travel from the eye to the relevant area of the brain.
For 90 days, half of the participants were given clemastine fumarate, and the other half received a placebo. Next, the groups were switched: the placebo group was given the drug and vice versa. Neither the participants nor the researchers knew which individuals were receiving the active treatments.
The analysis showed that the drug increased the speed of the neural signals from the eye to the back of the brain. Even once the experimental group stopped taking the medication and moved on to the placebo, the increased speed persisted.
“People thought we were absolutely crazy to launch this trial,” comments Prof. Chan, “because they thought that only in newly diagnosed cases could a drug like this be effective – intuitively, if myelin damage is new, the chance of repair is strong.”
In the patients in our trial the disease had gone on for years, but we still saw strong evidence of repair.”
Prof. Jonah R. Chan
Assessing myelin regrowth
In the current study, the researchers were not able to measure myelin regrowth using MRI scans. However, this is primarily due to limitations in technology, and as Prof. Chan says, “We still don’t have imaging methods that have been proven to be able to detect re-myelination in humans.”
Regardless of this, the evidence that re-myelination occurred is strong; there are no alternative explanations as to how VEPs could have increased.
Also, in vitro studies in human cells have shown that clemastine fumarate can stimulate activity in oligodendrocytes, which are cells that produce myelin in the central nervous system.
There is still a long path ahead, but the results are encouraging. Dr. Green is cautious not to jump the gun, saying, “By no means do we want to suggest that this is a cure-all.” But, it is difficult not to be excited at the potential of this drug.