Emeritus professor Jan Hoeijmakers is studying how DNA damage influences the development of dementia and ageing in various forms. His focus in particular is on children who have suffered from cancer.
NAME: Jan Hoeijmakers
STUDY: Molecular biology (Radboud Universiteit), PhD (Universiteit van Amsterdam)
CAREER: Emeritus professor and researcher, Department of Molecular Genetics Erasmus MC
You recently received your emeritus status, but will continue to do research. How so?
‘My emiritus is because of my age. But it affords me the ability to focus on research. I’m all refreshed and happy to be done with all the consultative committees – meeting this, debate that, phone call here, budget meeting there. Although everyone gets to a point where it’s their turn to take on these jobs, I’m a researcher first and foremost, and it’s a breath of relief to get back to doing research. For one thing, I’d like to focus on children’s cancer. Chemotherapy speeds up the ageing process, and we believe something can be done.’
What piqued your interest about age-related diseases such as dementia and Parkinson’s?
‘When I started at the medical faculty in 1981, I did not focus on common ageing diseases among older people, I focused on the opposite: particularly rare diseases in very young children afflicted by hereditary conditions dat will cause DNA repair to malfunction. Some of these diseases lead to specific types of cancer in children. Other children won’t develop physically or mentally and won’t age beyond twelve. In the early eighties, we were the first to isolate a human DNA repair gene. Once we knew how to, we isolated many more, and found the ones that were defective in these children. In the years after 2000 we managed to generate mice with the same defects these children had. And what happened? They went grey, developed a hump and osteoporosis, and their liver, kidneys and brains aged incredibly fast. On closer inspection, these brains showed a lot of similarities to those of patients with Alzheimer’s and Parkinson’s. But it took a lot of effort to convince the outside world that what had occurred really qualified as ageing and dementia. The ‘ageing community’ refused to believe our mice could age in three to five weeks. The magazine Aging Cell even published a satirical poem about our study.’
‘If you feed mice thirty percent less than normal, their life expectancy triples’
How can Alzheimer’s and Parkinson’s diseases be prevented?
‘This goes for both Alzheimer’s and Parkinson’s - you’re not born with it. It will take at least forty, fifty years to develop. The primary risk factor is ageing. What we can do, is slow down the ageing process, for instance through diet restriction. If you feed the fast-ageing mice thirty percent less than normal, their life expectancy triples. The greatest delay occurs in the nervous system. Eating less causes the body to de-prioritise growth in favour of immunity and maintenance, which means you’ll get to enjoy your body for longer. The thing that benefits in particular is the nervous system.’
So if I don’t eat too much at a young age, I decrease my chances to get dementia and Parkinson’s?
‘Right, you can do something about it now! Eat a healthy diet, but not too much. You’ll stay healthy for much longer. In Japan, children are taught to stop eating as soon as they feel they’ve had enough. That might explain why people in Japan reach such advanced ages. And it makes sense to moderate food intake. In the old days people had to eat more than they needed whenever food was around, to build reserves for days when there would be none. In our day and age we still act as if there won’t be enough food available tomorrow, when that’s not the case. So we constantly overeat. Age-related diseases are largely prosperity-related. You can’t prevent them altogether, but you can postpone them. For our research we’re collaborating with the Erasmus MC research institute Ergo, which monitors seniors in the Rotterdam borough of Ommoord. They get the people with the age-related diseases, we have the mice. We could generate a mouse that matches the diseases or handicaps they’re confronted with among people in Ommoord, to find out more about how it happens and what we might do about it. After all, that’s how it went with the children.’
What urges you to keep on doing research after your emiritus?
‘Curiosity. And my most important motive is to translate our research into improved wellness and health among all people. In this day and age, ageing-related diseases are a primary issue in healthcare, in terms of wellbeing and finances. It’s important that people age well, stay healthy and enjoy their lives. I also want to protect children who survived cancer from ageing prematurely. If through my work I get to contribute to their wellbeing, I’ll be quite happy.’
TEXT: Sjoerd Wielenga
PHOTO: Ruud Koppenol