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.

Contact

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

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Department Mitochondrial Proteostasis

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Department Biological Mechanisms of Ageing

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Gene therapy for mitochondrial diseases

Scientists alleviate disease symptoms in mice

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All cells in the body have the basic ability to protect themselves from infection, called the innate immune response. But how cells do this is not very well understood. Recently, scientists from the Max Planck Institute for Biology of Ageing and the University of Cologne, found that the size of the nucleolus plays an important role in protecting cells against infection.

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Crowding in the skin

Stem cells sense neighbourhood density to make decisions on their behaviour

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Nucleolus is a life expectancy predictor

Scientists discover that nucleolar size correlates with health and lifespan in organisms as diverse as roundworms, flies and humans

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More functional DNA in mitochondria cures male infertility

Higher number of mitochondrial DNA-molecules can compensate for negative effects of mutations

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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.

Head of the CRISPR Screening Platform (m/f/d)

Max Planck Institute for Biology of Ageing, Köln June 17, 2019

Five Master Fellowships

Max Planck Institute for Biology of Ageing, Cologne March 12, 2019

Postdoctoral Research Fellows (m/f)

Max Planck Institute for Biology of Ageing, Cologne January 09, 2019

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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Gut-microbes are key regulators of host’s life span and ageing

2017 Valenzano, Dario Riccardo

Cell Biology Developmental Biology Evolutionary Biology Genetics

Gut microbes impact host physiology, affecting health status, and imbalance of the gut microbial commensal communities is associated with disease. Re-establishment of a healthy gut microbial composition can resolve acute and life-threatening bacterial infections. Recent work using the short-lived African turquoise killifish (Nothobranchius furzeri) indicates that gut microbes from young individuals can modulate the general health status and life span in healthy ageing subjects.

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Ageing is not a random process. Biological ageing processes are instead regulated by metabolic and genetic mechanisms. Single gene mutations can markedly extend the life span of various organisms. The biology of ageing can be investigated in simple yeast cells, flies, round worms, and also in mice. Gene mutations that extend life span also protect against age-associated diseases such as neurodegeneration, cancer, heart disease, and diabetes. A deeper understanding of molecular mechanisms of longevity can open new avenues for therapies or prevention of these highly relevant diseases.

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Studying adult stem cell regulation using skin as a model

2015 Wickström, Sara A.

Cell Biology Developmental Biology Evolutionary Biology Genetics

How complex but stereotyped tissues are formed, maintained and regenerated through local growth, differentiation and remodeling is a fundamental open question in biology. To answer this question we need to understand how single cell behaviors are coordinated on the population level and how population-level dynamics are coupled to tissue architecture. Uncovering these regulatory principles will further facilitate development of stem cell therapies and effective treatments to slow down ageing and prevent age-related diseases such as cancer.

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A naturally occurring metabolite prolongs life

2014 Denzel, Martin S.; Winnen, Brit; Antebi, Adam

Cell Biology Developmental Biology Genetics Structural Biology

During ageing, human proteins tend to aggregate. At a certain point, protein aggregation becomes toxic, which can cause damage to occur also in neurons and may result in neurodegenerative diseases. By studying model organisms like the roundworm Caenorhabditis elegans, it is possible to uncover the mechanisms underlying neurodegeneration. Scientists recently found that a naturally occurring molecule enhances defence mechanisms against neurodegenerative diseases. Feeding this particular metabolite to C. elegans improves clearance of toxic protein aggregates in the body and extends life span. 

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