Björn Schumacher

Björn Schumacher
Affiliation: University of Cologne, DE


Keywords: Genome Stability in Ageing and Disease




Full profile:
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.