Welcome to the Leibniz Institute on Aging (FLI)
The Leibniz Institute on Aging – Fritz Lipmann Institute (FLI) is the first national research institute in Germany focusing on biomedical research on human aging, a multifactorial process controlled by environmental and genetic factors.
This website will provide you with an insight into our institute, the research we do and the faces behind FLI's science activities. We wish you an exciting and entertaining voyage of discovery into the world of aging research at FLI.
Since 2004, our mission has been to delineate basic molecular mechanisms that underlie the aging process in humans and its consequences for the development of aging-related cell and tissue dysfunction and diseases. Research at the FLI will provide a knowledge basis for the development of therapies aiming to facilitate healthy aging by prolonging organismal functions and disease prevention in the elderly.
In order to better correspond to this research focus, the institute was re-named from Leibniz Institute for Age Research into Leibniz Institute on Aging in 2015.
recent high impact publications
- Impaired planar germ cell division in the testis, caused by dissociation of RHAMM from the spindle, results in hypofertility and seminoma.
Li H, Frappart* L, Moll* J, Winkler* A, Kroll T, Hamann J, Kufferath I, Groth M, Taudien S, Schütte M, Yaspo ML, Heuer H, Lange BMH, Platzer M, Zatloukal K, Herrlich P, Ploubidou A
Cancer Res 2016 (epub ahead of print) * equal contribution
- Prediction of conserved long-range RNA-RNA interactions in full viral genomes.
Fricke M, Marz M
Bioinformatics 2016 (epub ahead of print)
- Metabolic regulation of stem cell function in tissue homeostasis and organismal ageing.
Chandel NS, Jasper H, Ho TT, Passegué E
Nat Cell Biol 2016, 18(8), 823-32
- Multifocal Nerve Lesions and LZTR1 Germline Mutations in Segmental Schwannomatosis.
Farschtschi S, Mautner VF, Pham M, Nguyen R, Kehrer-Sawatzki H, Hutter S, Friedrich RE, Schulz A, Morrison H, Jones DTW, Bendszus M, Bäumer P
Ann Neurol 2016 (epub ahead of print)
- Different promoter affinities account for specificity in MYC-dependent gene regulation.
Lorenzin F, Benary U, Baluapuri A, Walz S, Jung LA, von Eyss B, Kisker C, Wolf J, Eilers M, Wolf E
Elife 2016, 5 doi: 10.7554/eLife.15161
- DNA damage tolerance pathway involving DNA polymerase ι and the tumor suppressor p53 regulates DNA replication fork progression.
Hampp S, Kiessling T, Buechle K, Mansilla SF, Thomale J, Rall M, Ahn J, Pospiech H, Gottifredi V, Wiesmüller L
Proc Natl Acad Sci U S A 2016, 113(30), E4311-9