CECAD

»We Have to Improve Our Understanding of the Aging Process«

Interview with Aleksandra Trifunovic

Our life expectancy keeps getting longer – thanks in part to research on aging. Professor Aleksandra Trifunovic, Principal Investigator and acting director at the Cluster of Excellence on Aging Research CECAD, searches for molecular causes of aging ­associated diseases. Her research is not about further increasing our life span, but rather about enabling a longer healthy life.

How close are we to getting a pill to stop us aging?
(laughs) It depends on what you mean by stopping aging. Aging research does not aim to prolong the human lifespan for another hundred years. What we are trying to do is to stop aging-associated diseases to prolong the healthy lifespan, so that at the age of 80 you are still healthy and not suffering from different diseases. Unfortunately we are still quite far from reaching that goal, but there is a huge scientific community working on the problem, and we are finding out new things almost every day. As we speak, there is some new development. The problem is, aging is very complex and complicated. I am very skeptical that we will ever find a single pill to stop all this.

Where do you see the greatest challenges of aging research in general?
The greatest challenge is the complexity of the process, because we are not working on one single disease, we are working on many disease and on different levels. Aging-associated diseases are everything from neurodegenerative diseases like Parkinson’s or Alzheimer’s to different types of cancer, type2 diabetes and the like. Basically every organ system in our body changes with aging and can acquire different diseases.

Pseudoscience and quacks play a major role in the public perception. How can you fight this?
This in unfortunately very true. Every now and then new things pop up that are basically pseudoscience. Some examples are the widespread obsession with a gluten-free diet, detox smoothies and so on. There is a little bit of science in it and then it becomes pseudoscience. We have to be much more engaged, more present in the public.

Can you give an example of what you can do?
We need to engage children and young people, open our doors to allow people to understand what we are doing, be more present in the press. Something most scientists are not really exploring are the new ways of communicating to the public. We still stick to our papers, and interviews and TV as media, but there are so many more things out there. We should try more: Instagram, Facebook and other ways of communicating. Scientific blogging is also important – this could be one way to communicate more with younger people and to people trying to find answers on the internet. You see many pseudoscientific blogs, promising that with the right diet you will stop aging. We should fight on their field and increase our visibility.

We are getting older and older. This also leads to greater questions. How do we want to live our life? Who is going to care for us? Who is going to pay? Which solutions do you see?
Research with the aim of prolonging the healthy lifespan can help society shoulder this challenging burden of increasing health costs for an aging population. This pertains to things like our pension systems or our old-age care systems. Across Europe, societies are facing similar challenges. But if we can prolong the health span, we might also need to prolong the work span. I do not think that in the long run, with a continually increasing lifespan, we can continue to finance the current systems.

Aubrey de Grey is a bioinformatican living in Cambridge. In his book, The Mitochondrial Free Radical Theory of Aging, he claims we could stop aging by deleting damage of the mitochondrial DNA. What is your opinion of him and his research?
I have known Aubrey personally for years. He is a remarkable person, as he managed to get a lot of people aboard, to get a lot of funding for research into aging. However, I believe that he also does a lot of damage to the field. He claims that he has an excellent plan to cure aging, and that scientists just don’t listen to him. Of course, this is not true.
He has the idea of approaching aging as you would an old car, by replacing different parts. He claims that we could basically stop aging and might live a thousand years if we followed his guidelines, which are very simple. However, the problem we are facing is not simple at all. We still do not understand the molecular mechanism behind aging. In fact, we still do not understand all the different factors contributing to the process. Therefore, what he proposes is far from reality. At this point, it is just science fiction.

With CRISPR/Cas9, a new technology is on the rise that might change a lot. This molecular biological method makes it possible to cut out or change specific genes with a “gene scissor” of sorts. Where do you see aging research ten years from now?
First: we need to understand the aging process itself better. CRISPR for the first time gives us the chance to change things in a single animal, and that is amazing. It will impact science on all different levels, in all different parts, in all different disciplines. In aging research as well, CRISPR will play an important role. Initially it will be more important for monogenic diseases, where there is one mutation and you can fix the problem. Aging is so complex that it is not one of the first things we are going to be able to fix with CRISPR.

Your daughter started secondary school. How do you explain to her what you do every day?
Children in general are curious and love experiments. My daughter is no different. At home we extracted DNA from strawberries once. She and her friend were so impressed. She does not really know in detail what we do, but she often visits the lab. A couple of years ago we had her whole class visiting us for a few hours – and they all wanted to stay for a whole week afterwards. It is great how kids see the world and ask questions. One of her friends saw the roundworm C. elegans with red fluorescence under the microscope. We told them that a protein taken from jellyfish is what makes the worm red. The kid said: “It’s like when flamingos eat crustaceans and turn pink, isn’t it?” It was a great idea. It shows that kids are really into science and think about what you show them.

 

Can you outline what your research is about?
Personally I am interested in mitochondria. They are present in every cell of our organism and make almost all of the energy for us. The amount is amazing. They produce about 70 kilograms of the energy carrier adenosine triphosphate (ATP) – every single day. That is almost the equivalent of our body weight. Mitochondria were once bacteria. They invaded our cells and stayed there, allowing us to use oxygen and produce much more energy. This was the boom that allowed multicellular organisms to appear. The problem is: this symbiosis came at a cost. Mitochondria accumulate mutations over time and produce reactive oxygen species, also known as free radicals, that can be harmful. Today we know that this is also important for signaling purposes. I work on basic molecular mechanisms how mitochondria communicate with the cell, and how this changes during aging and in certain diseases. These diseases mainly affect neurons and muscles. This, in turn, is connected with the aging process because those tissues have the most problems with aging. Each mitochondrial disease on its own is rather rare. But taken together, they affect one in 3,000 people. In children they are approaching the same number as childhood cancers.  However, we are not sure which aspects of the normal aging process are caused by mitochondrial DNA mutations. We know that they accompany aging and that they increase with age. But is it five percent they contribute to the aging process, or ten, or twenty?

What do you think: Will there be a pill against mitochondrial diseases in five, ten or twenty years?
Similar to aging, mitochondrial diseases are very broad field and can affect different organs. We cannot really fight all of them together – but maybe in groups. There are new treatments. Unfortunately we do not have a single treatment to cure the disease. We are still only ameliorating the symptoms. I do not want to venture any predictions in years, it is not good to get people’s hopes up, but every single day there are new ideas and new results. So I think it will be “soon.”

You seem to be a European prototype: born in Montenegro, studied in Belgrad, then you moved to Stockholm and now you are in Cologne. Of all the different countries, where do you see the greatest differences in aging and aging research?
I feel at home in four cities and countries. Sweden and Germany are quite similar, because Sweden has one of the longest-living populations, closely followed by Germany. Germany has more specific centers focused on research into aging, because it is bigger and research is more massive – likely it is the best place in Europe right now for research. In aging research we are definitely at the forefront.

CECAD hopes to be part of the next round of the Excellence Initiative. Why should CECAD take part?
I was recruited in the early period, and you can see how CECAD has changed the whole university campus since 2009. In the second round of the Excellence Initiative the University of Cologne received funding, and part of that success is due to CECAD. It managed to bring together a really international group of people working on the same topic and was very successful at it.

If you had three wishes for CECAD, what would they be?
First: Get the grant – that is everybody’s wish. Not because we would get more individual funding, but because it would change everything around us. We could recruit new people and invest into even better core facilities. Second: I would like CECAD to become a globally renowned research institute. Here we are already headed in the right direction. Third: I would like us to be able to recruit and fund young people. Only with young people we can flourish, get new ideas and develop new research.