Prof. Dr. K. Lenhard Rudolph
Group Leader
Our current work focuses on the influence of early life growth signals on the pace of aging, particularly the development of aging-associated metabolic alterations that limit the function of stem cells and organ function.
We aim to delineate the potential of new interventions to reverse aging-associated impairments in metabolism and nutrient stress responses to improve healthy aging.
Researchers from the Leibniz Institute on Aging – Fritz Lipmann Institute (FLI) in Jena, Germany, and the Fred Hutchinson Cancer Center, Seattle, USA, have succeeded in developing a novel method that makes genetic analyses possible for all regions of the intestine. This will facilitate future research on how genes influence the normal function of the intestinal lining, as well as their effect on diseases and aging.
From June 29-30, 2023, the annual meeting of the DGfA took place in Jena. With 3 fantastic keynote speakers, a selection of short talks, numerous interesting posters and the chance for networking and socializing, this meeting offered the over 170 international participants many opportunities for scientific discussions.
Throughout one’s life, the blood is constantly being replenished from blood stem cells. However, these cells lose their functionality in old age. Researchers at the Leibniz Institute on Aging – Fritz Lipmann Institute (FLI) have now found a gene mechanism that is responsible for the aging of hematopoietic stem cells. The gene Igf2bp2 is important in youth for the full function of these cells, as it activates their growth and metabolism. When the gene is missing, however, the aging-associated loss of function of the stem cells is surprisingly diminished. The eventual aging of hematopoietic stem cells is apparently already preprogrammed by their gene-driven growth in youth.
Researchers from the Leibniz Institute on Aging - Fritz Lipmann Institute (FLI) in Jena combined the use of mouse pluripotent stem cells and flatworms to identify genes that control lifelong maintenance and regeneration of tissues. Flatworms (also known as planarians) possess immortal regenerative capacity. Now it was discovered that the induction of fat metabolism by the Tnfaip2 gene promotes the ability of stem cells to produce differentiated organ cells. When the gene is lost, planarians lose their capacity of organ maintenance and regeneration. Disturbances in fat metabolism may also contribute to the loss of organ maintenance and to cancer development at old age.
