Johan Ericson: Our Stem Cells may be 10 Times More Effective

As early as the 1980s and 1990s, transplantation trials were conducted using fetal tissue from aborted fetuses to replace lost dopamine cells. The results were mixed, but in some cases remarkable. Some patients experienced significant improvement, and in the most successful cases, people with severe Parkinson’s symptoms were able to return to a much more normal life.

"There are patients from those studies who experienced significant improvement. In some cases, they were able to stop symptomatic treatment and return to a more normal working life." says Ericson.

This is important, he emphasizes, because it means one thing: "We actually have a 'proof of concept' in humans. We know that the principle, that is, replacing lost dopamine cells, can work."

The problem was that this approach could never become a large-scale treatment. The supply of tissue was limited. The biology was difficult to standardize. The model was both practically and ethically challenging.

Ericson's Stem cells change that.

In principle, they make it possible to produce large quantities of cells under controlled conditions, with defined quality and a higher degree of standardization. That is why this field is now once again seen as vibrant.

But this is not the same as saying that every stem cell-based approach will succeed: "The crucial question is whether the cells we create actually meet the required quality standards. Do they behave like the body’s own dopamine neurons? Do they survive? Do they mature properly? Do they integrate into the network? That is what we are trying to document."

His own claim is that they come closer than others. Not because the idea is new, but because the quality of the cell product is higher. He believes their method yields a significantly higher proportion of therapeutically useful dopamine cells than previous approaches; in interviews, he speaks of up to ten to twenty times higher yields of relevant cells.

If that’s true, it’s not a minor detail. It’s the whole difference.

What the field has struggled with

It’s rare for researchers to speak so bluntly about one another in public contexts, but there is a clear conflict in Ericsson’s account.

The field has, as he sees it, long used methods that are similar to one another. The basic idea has been the same. But the yield of the cells one actually needs, the dopamine neurons, has often been low. In practice, it can be as low as 2 to 10 percent.
The rest are other cells. Immature cells. Irrelevant cells. Cells that take up space without providing the desired therapeutic effect.

"If the product consists mainly of other cell types, they take up space in the brain without providing the desired therapeutic effect. In the worst case, an oversized graft can cause tissue damage, even if it doesn’t result in cancer or tumor formation."

It is this part of the presentation that makes the strongest impression. Not the grandest promises, but the dry logic: If you are going to replace lost dopamine neurons, you actually need to have enough of them. Not just a vague cocktail of cells that might do something useful.

Thus, his project is less about a spectacular idea than about strict quality control.

Quality over quantity

This is also how he explains the dosage issue. Most clinical trials currently underway have, roughly speaking, given patients between 2 and 15 million cells in total. But, he points out, the decisive factor is not just the number. If the quality is high, you don’t necessarily need enormous quantities.

"There are approximately 300,000 dopamine cells per hemisphere in the relevant system, so in theory you don’t need enormous quantities if you actually have the right cells. In addition, there are different subtypes of dopamine neurons, and the A9 subtype in particular is important for the motor symptoms of Parkinson’s. This makes it even more complicated."

So it’s not just about how many cells you implant.

It’s about what kind of cells they are.

The toughest questions

This is where journalistic instinct must kick in. Because it’s easy to get carried away by the narrative: dead cells are replaced with new ones. The brain is repaired. The future is brought forward.

But biology is full of elegant ideas that have run aground between rats and humans.

The common counterargument is that there is a big difference between rats and humans. Many things look promising in preclinical trials and fall apart in clinical studies.

"That’s absolutely right, and that’s why we have to be cautious. But here we have an extra point of reference, because there is already historical data in humans showing that cell transplantation can work. The question is whether the stem cell product is good enough."

This is the point where most promising ideas in medicine face their toughest test: the transition from model to human. "The biggest uncertainty is always what happens when the cells do what we hope they will after they enter the human brain; they must survive, mature, produce dopamine, and integrate into the system in a meaningful way. And they must do so without causing problems."

On one of the last slides is a single word:

Safety.

Below it: a short list. Wrong cell types. Overgrowth. Undesirable effects. Tumor formation. Space issues in the brain.

"The brain is already full. If one introduce cells that not only do their job but also take up space they shouldn’t, that in itself can become a problem."

It’s a reminder of what makes this research so demanding. Not only must you create the right cells, but those right cells must behave correctly, in the right place, in the right numbers, over a long period of time, within one of the body’s most complex organs. This is not a treatment that can be turned off or adjusted afterward. It is a surgical intervention.

And even though many of Parkinson’s most well-known symptoms are linked to dopamine, Parkinson’s is more than a dopamine disorder. It is also a disease with non-motor symptoms, various subtypes, and a biology that has not yet been fully mapped. Even if we succeed in replacing dopamine cells, that does not necessarily mean that all aspects of the disease will disappear.

"I don’t think a single treatment will solve everything about Parkinson’s. The disease is more complex than that. But if we can restore the dopamine system that has been lost, we can push the boundaries of what is possible quite significantly."

Human trials that make the field hard to dismiss

Clinical studies are already underway globally. The field is no longer in the conceptual stage. Both embryonic stem cells and iPS cells are being used in projects that have entered the early clinical phase.

Ericson isn’t first in line. He knows that. He emphasizes it himself: “We are by no means the first on the scene. But we believe we may have a better method.”

He points in particular to a study from South Korea, which he describes as very promising.

“When their preclinical study came out, I saw right away that the grafts looked better than what you usually see.” They have now evaluated the first year in twelve transplanted patients, and all twelve have shown symptomatic improvement. The group that received the most cells appears to have had an even better clinical effect. This is an important signal that this type of therapy may actually work in a significant proportion of patients.

It is not definitive proof. But it is enough to make it difficult to dismiss the entire field as wishful thinking. The principle can work. The question is how well, how safely, and for whom.

This is also where Ericsson’s claim to be 'best in class' makes some sense. He isn’t saying they are first. He is saying they can be better.

Who will be able to benefit from this treatment?

Another question naturally follows: Who is this treatment actually intended for?

Not necessarily the very sickest patients. Not necessarily those who have only had mild symptoms for a short time. Rather, somewhere in between: "As it stands now, likely patients in the middle of the disease course. Previous results suggest that it may be best to treat relatively early. If you wait too long, the response may be poorer."

At the same time, the first clinical trials will always be cautious, precisely because you have to measure both efficacy and assess safety.

"The first studies are always conservative, because it can be dangerous; it can go wrong. You need to know if tumors, overgrowth, or other unwanted effects occur. That’s why you don’t start with the very sickest patients."

This makes the project less straightforward than the immediate narrative suggests. This is not “one operation and the problem is solved” kind of thing. It is more accurate to say that he is attempting to make it biologically possible to restore some function to selected patients—initially, likely in carefully defined groups.

Nevertheless, it is difficult to escape the underlying drama. For in a field of medicine where so much revolves around delaying, slowing down, adjusting, and managing, this carries a different kind of promise.

Not that time will be stopped.

But that something lost can be rebuilt.

When asked whether this can, at best, make patients “almost healthy,” he weighs his words before answering:

"People are often cautious about using the word “cure,” and that’s understandable. But in the most successful historical transplant trials, there were indeed patients who improved so much that they could stop symptomatic treatment and return to a normal working life. So in an optimal scenario, you can go very far."

He stops there. Not because he doesn’t see the greatness of what he’s working on. But because he’s a scientist enough to know the difference between hope, a principle, and a treatment.

What will the future bring

Outside, Oslo carries on at its own pace. Trams, taxis, people with shopping bags, office workers on their way home, tourists stopping at the entrance to take a picture of the facade.

Inside the conference rooms, a portrait interview has focused on something that just a few decades ago would have been pure speculation: cultivating new brain cells and implanting them into a damaged nervous system, not to alleviate symptoms from the outside, but to rebuild some of what has been destroyed.

No one knows yet how far this will go. Not even Ericson. He is too much of a researcher for that.

But if he succeeds, Parkinson’s will no longer be just a disease one tries to live with for as long as possible.

Then it will also be a disease where some of what has been destroyed can actually be rebuilt.