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Thomas Willnow: Funding for risky projects

Thomas Willnow analyzes the connections between metabolism and dementia. We asked him why European funding is essential to his research and why he considers it to be risky.

Prof. Thomas Willnow. Image: David Ausserhofer/MDC

What makes ERC grants special?

The ERC was a quantum leap for research funding in Europe. Previously, the focus was on strategic collaboration, since the EU wanted to strengthen networking. The ERC takes an entirely different approach. Here it’s not about funding consortia, but about supporting a single person or research team, and about having a good idea and implementing it. The assessments are transparent and are of a high scientific quality. The reviewers select a handful of people and entrust them with a lot of money, even if the projects are risky. The only comparable funding available to researchers in Germany is the Leibniz Prize. The prestige is correspondingly high. This helps initially but it brings with it responsibility. Five years down the road, people look very closely at what the laboratory has actually done with the two and a half million dollars.   

What is “risky" about your project? 

Our project focuses on the metabolic causes of neurodegenerative processes. The questions behind this research are eminently important. The study of patient groups has shown a link between metabolic disorders and the risk of dementia. Yet just how blood vessels or the liver or fat tissue, for that matter, interact with the brain remains unclear, as does why the risk of developing Alzheimer’s disease is higher. But this knowledge is essential to assessing risk factors and to finding a new approach to dementia therapy. Patients with metabolic disorders can make considerable gains if they change their lifestyle, adjust their diet or take medication. So rather than trying to rescue nerve cells, the onset of age-related dementia should be fought by minimizing metabolic risk factors.

But the problem is that although this has been known for years in genetics, so far no one understands the link. We want to use mouse models with metabolic diseases to study the risk of developing neurodegeneration. But is this at all possible? Are mouse models with metabolic disorders suited for identifying this link? That is a risk we are taking.

Do you have any preliminary results?

Yes, we have actually been able to demonstrate this link for certain metabolic regulators. The question is now whether one can use this knowledge to halt or minimize neurodegenerative processes via these signaling pathways. This remains to be seen. In the two years since the project began, we have at least gained a mechanistic understanding of the link between metabolic changes associated with obesity and the signaling pathways that support the survival of neurons.

Background: Prof. Thomas Willnow's group "Molecular Cardiovascular Research" analyzes fundemental processes of cell biology. These are relevant for neurodegenerative and metabolic diseases as well. 

Further information on the ERC Grants at the MDC