Björn Schumacher


Also Known As
Head of Research Area 2, Institute for Genome Stability in Ageing and Disease, Faculty of Medicine

Prof. Dr. Björn Schumacher’s research group uses the nematode worm Caenorhabditis elegans to understand the causal role of DNA damage in aging and disease. With increasing age, damage to the genome accumulates and leads to the degeneration of cells and tissues. DNA damage thus plays a causal role in aging-associated diseases. The risk of cancer also increases with age because erroneously repaired DNA leads to mutations that can trigger cancer. Schumacher’s team has identified mechanisms that antagonize the detrimental consequences of DNA damage by maintaining tissue integrity and maximizing lifespan, even when the DNA damage cannot be repaired. The Schumacher group has also shown that DNA damage in individual cells impacts the entire organism. The systemic DNA damage responses are mediated by the immune system and increase the general stress resistance of the tissues throughout the body. These findings are particularly important for understanding progeria, disorders that result in premature aging in childhood. Premature aging is caused by congenital dysfunction of the DNA repair processes. Understanding the mechanisms by which organisms respond to accumulating DNA damage with age is pivotal for developing novel therapies to prevent aging-asso-ciated diseases and contribute to optimizing cancer treatment. Our research: The DNA in each cell of the human body experiences many damaging influences over a lifetime. Although the cells have very effective DNA repair mechanisms, DNA damage inevitably accumulates with age. DNA damage leads to a loss of tissue function and the onset of aging-associated diseases. Prof. Bjorn Schumacher’s research group explores how DNA damage affects cells, tissues, and the organism as a whole. This research is important in understanding several congenital diseases caused by defects in the highly complex nucleotide excision repair pathway (NER), including the childhood progeroid (premature aging) diseases, Cockayne syndrome (CS) and trichothiodystrophy (TTD), and xeroderma pigmentosum (XP), which increases the risk of skin cancer. Better understanding of the consequences of DNA repair defects may also lead to new therapeutic options for aging-associated disorders and cancer. Our success: Prof. Schumacher’s group has shown that organisms respond to DNA damage by activating genetic mechanisms that prolong life. The focus is on understanding how this response to DNA damage is regulated so that the organism can maximize its survival even if the DNA cannot be repaired. Schumacher’s team has already identified mechanistic links between the ge-netic aging process and the stochastic accumulation of DNA damage. Schumacher and his team have revealed a previously unknown systemic immune response in C. elegans. Their key finding is that an immune response activated in individual cells in response to DNA damage can be transmitted throughout the entire body to promote survival of the organism in the face of further stress. Prof. Bjorn Schumacher has been awarded the Innovation Prize from the State of North Rhine-Westphalia, holds the ERC starting grant and coordinates the European training network “CodeAge” on chronic DNA damage responses in aging. Our goals: Understanding the fundamentals of the aging process is essential for developing new therapies. It is well-known that cancer can be the result of DNA damage. Schumacher’s team recently discovered mechanisms through which the entire body responds to DNA damage in specific cells. The organism increases its chances of survival by complex systemic physiological changes. The Schumacher group aims to investigate the regulation of these systematic responses to genome damage. The ultimate goal is to support the development of novel therapies for aging-associated diseases and rare progeroid syndromes. Our methods/techniques: The nematode C. elegans allows scientists to gain insight into the processes of DNA repair and aging, thus revealing how cells, tissue, and the body as a whole respond to DNA damage, how the organism ages, and what mechanisms may prolong survival. The C. elegans research is complemented by extending the studies to mice to address disease-specific questions. The mouse models reflect complex diseases very well, allowing researchers to explore novel therapeutic options for humans.

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