Max Planck Institute for Biology of Ageing

Max Planck Institute for Biology of Ageing

All humans age – just like almost all other living organisms. One reason is that the genetic material, the DNA, is increasingly damaged over time in every cell. Scientists at the Max Planck Institute for the Biology of Ageing study how cells age during their lifetime and examine which genes and environmental factors are involved in the process.

The scientists employ molecular-biological and genetic techniques to explain the fundamental processes on the basis of model organisms, such as mice, fruit flies and threadworms. These animals are particularly suitable as their genomes are well understood and they have a relatively short life expectancy. It is known, for instance, that the life expectancy of a threadworm is influenced by around 100 genes and that insulin signal transduction is involved in the ageing of its cells. Researchers are certain that similar processes also influence ageing and life span in human beings. In the long-term, basic research is expected to contribute to people being able to enjoy longer and healthier lives.


Joseph-Stelzmann-Str. 9b
50931 Köln
Phone: +49 221 37970-0
Fax: +49 221 37970-800

PhD opportunities

This institute has an International Max Planck Research School (IMPRS):

IMPRS on Ageing

In addition, there is the possibility of individual doctoral research. Please contact the directors or research group leaders at the Institute.

Department Molecular Genetics of Ageing


Department Mitochondrial Proteostasis


Department Biological Mechanisms of Ageing


Department Neurobiology of Ageing

Molecular structure of the mTOR complex

Endogenous metabolite directly inhibits mTORC1 activity

Historical drawing of wave

How a single enzyme unleashes a complex DNA repair process

The picture shows a collection of cells under the microscope.

Study on mice shows male-specific effects on health

The image shows cells under the microscope that glow fluorescently.

Coenzyme Q distribution within the cell is regulated by mitochondria

Two fruit flies sitting on a pill.

Studies in fruit flies reveal how the sex determines the responses to the anti-ageing drug rapamycin

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Linda Partridge and her colleague Sebastian Grönke at the Max Planck Institute for Biology of Ageing in Cologne can’t promise eternal life – but they are at least discovering ways to lead a healthier one. The researchers’ findings in fruit flies and mice have revealed astonishing new insights into ageing that will also benefit us humans.

Life is short, especially for the turquoise killifish, Nothobranchius furzeri: it lives for only a few months and then its time is up. During that short life span it passes through every phase of life, from larva to venerable old fish. Its brief life expectancy – unusual for a vertebrate – has long fascinated Dario Valenzano of the Max Planck Institute for Biology of Ageing in Cologne. In just ten years, he has turned it into a model organism for research on aging.

12 fully funded PhD positions (m/f/d) | Ageing Research

Max Planck Institute for Biology of Ageing, Cologne August 16, 2023

A quest for the elixir of youth

2022 Lu, Yu-Xuan; Partridge, Linda

Cell Biology

Imagine you could take a medicine that combats the ill health that comes with age, and keeps you living healthily for longer. Scientists are trying to find a drug that has these effects. The current most promising anti-ageing drug is Rapamycin, known for its positive effects on health and lifespan in laboratory animals. However, potential negative side effects and a lack of clinical data for its effects hold back its usage as a geroprotector. Our findings are helping to understand how this drug works, to open new doors for a potential application in humans.


Fountain of youth for ageing stem cells in bone marrow

2021 Tessarz, Peter

Cell Biology Genetics

As we are ageing, our bones become thinner, we suffer fractures more often, and bone-diseases such as osteoporosis are more likely to occur. One responsible mechanism involves the impaired function of the bonemarrow-resident mesenchymal stem cells, which are required for the maintenance of bone integrity. We now have been able to show that these changes can be reversed by rejuvenating the epigenome. Such approach could contribute to the treatment of diseases such as osteoporosis in the future.


The mitochondria – microbe conflict

2020 Li, Xianhe; Straub, Julian; Stillger, Katharina; Pernas, Lena

Cell Biology Evolutionary Biology Genetics

Mitochondria, essentially domesticated microbes in our cells, play a defensive role during microbial infection. In previous work, we showed that mitochondria can compete with the human parasite Toxoplasma gondii for fatty acids, thereby restricting its growth. Here, we further investigated the metabolic conflict between mitochondria and Toxoplasma. We report a novel structure we term SPOT - structure positive for outer mitochondrial membrane - that emerges from the outer mitochondrial membrane due to mitochondrial import stress caused by the Toxoplasma.


Rewiring of mitochondria in cancer

2019 MacVicar, Thomas; Langer, Thomas

Cell Biology Developmental Biology Genetics

Many cancers reprogram cellular metabolism in order to sustain tumour growth. Mitochondria are essential organelles which provide cancer cells with the metabolic flexibility required in challenging environmental conditions. Our recent work has revealed that tumour cells growing in low oxygen or nutrient deprived conditions are able to rewire their mitochondria by degrading specific mitochondrial proteins. We propose that analyzing this mechanism will provide therapeutic targets in hard-to-treat tumours such as pancreatic cancer.


Small protein modifications with high impact

2018 Matić, Ivan; Colby, Thomas; Burkert, Annegret

Evolutionary Biology Genetics

ADP-ribosylation (ADPr) is a protein modifier playing key roles in health and disease, from bacterial pathogenesis to cancer. Yet for decades it has been difficult to investigate the detailed mechanism of this modification. Using advanced proteomics, we discovered serine ADPr (Ser-ADPr) as a new and widespread protein marker needed for DNA damage response and were able to describe its biochemical basis by identifying its “writers” and “eraser”. These discoveries opened a large and novel research area into how ADPr regulates essential cellular processes.

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