Researchers say the destruction of these sheaths causes multiple sclerosis symptoms.
Scientists have suggesting that myelin repair in people with multiple sclerosis may be possible as long as certain cells still survive.
These cells, called oligodendrocytes, are acquired since birth and make up the myelin sheaths around the nerves that are destroyed by the disease.
The destruction of the sheaths causes symptoms associated with MS. Repairing myelin may be the only way to repair damage from the disease’s progression.
“People with MS do not generate cells needed for re-myelination. Instead their bodies depend upon cells given at birth,” Dr. Jonas Frisén, the lead study author and a professor of stem cell research at Karolinska Institutet in Sweden, told Healthline. “We need to save these cells.”
To obtain their data, study authors relied upon nuclear bomb tests that were conducted in the United States, Soviet Union, and other countries in the 1950s and 1960s.
The residue of the bomb tests released radioactive carbon into the atmosphere that spread around the globe.
The residue left a lasting mark on human cells. This marker was used, postmortem, to determine the age of cells.
“The results were a big surprise,” Frisén said. “This is technically difficult to approach in humans. There is no other source of a marker in the environment that is integrated in DNA and can be used for the analysis of cell generation. This is the first human study.”
What the researchers found was contradictory to previous thinking.
In mice models, it’s the new oligodendrocytes that repair the myelin. But in humans, it’s the old cells that come to the rescue.
“These results strengthen the support to treat MS aggressively and early in the disease to prevent loss of oligodendrocytes, which are not replaced efficiently. We need to save the ones we have,” Frisén said.
“This was a robust study containing about 40 MS tissues and about the same healthy tissues,” he said.
The postmortem samples came from tissue banks in the United Kingdom, United States, and other countries.
The study is changing the way experts think about treatment strategies.
“It means that prompting new oligodendrocytes is not a viable strategy,” Frisén said. “Instead, we need to keep them alive and functioning and trigger them to repair.”
“This is a very provocative paper,” Claude Schofield, PhD, director of discovery research at the National Multiple Sclerosis Society, told Healthline. “If it turns out to be true, it’s a pretty important finding.”
“This will have a massive impact on how we view our approach to treating MS,” Schofield added. “More research is needed. But measuring the age of cells is not available. If we could develop chemical markers (other than nuclear isotopes) that could date cells, it is possible to recreate and do the research needed.”
“This study was done postmortem with donated tissue. If we could develop markers to use with imaging techniques, we could better understand the pathology of individual MS and lead to better treatments,” Schofield said.
Not all oligodendrocyte cells are the same.
Some cells may create longer myelin sheaths or have other unique features.
These subgroups of cells were identified in a recently published in the journal Nature.
The findings may be important to understanding disease progression and developing therapeutic approaches.
“This is huge for MS,” Schofield said of the second study. “It will revolutionize the way we look at MS.”
Schofield explains how, up until this study, we could only identify a cell by its shape and other features. But with this new methodology, we’re able to see a fingerprint of the cell and know everything about it. He likened it to the difference between a rotary phone and today’s smartphones.
“Now we can find differences that we would never detect before,” he said. “In terms of understanding disease, this is the future, the most important thing going on in biology right now.”