Leibniz Institute on Aging - Fritz Lipmann Institute (FLI)
We conduct research on the biology of aging at the molecular, cellular, and systems levels.
A review article now published in “Nature Reviews Genetics” brings together evolutionary theory, comparative genomics and large-scale human genetics to explain why we age and why ageing rates differ among individuals and species. The two authors—from the Leibniz Institute on Aging—Fritz Lipmann Institute (FLI) in Jena and University College London in London—describe how, because modern humans now routinely survive into old age, we live with the late-life consequences of biological pathways that natural selection optimized for youth, and of harmful mutations that act too late in life for selection to clear them efficiently. Reading ageing through this evolutionary lens also clarifies why age-related diseases share genetic roots — and points to targeting a small set of ancient, conserved pathways to counter several of them at once.
Dr. Dario Lucas Helbing of the Department of Psychiatry and Psychotherapy at Jena University Hospital—a site of the German Center for Mental Health (DZPG)—has secured funding in collaboration with Prof. Dr. Helen Morrison of the Leibniz Institute on Aging—Fritz Lipmann Institute (FLI) in Jena. The research project “Identification and Validation of Causal Multimodal Molecular Signaling Pathways in the Spectrum of Depression and Neuropsychiatric Post-COVID Syndrome” will receive 25,000 euros in funding from the LIFE “Connect” Initiative at Friedrich Schiller University Jena.
Why does the gut microbiome lose its balance as we age? Researchers at the Leibniz Institute on Aging – Fritz Lipmann Institute (FLI) in Jena now present a new explanation in a paper published in “PLoS Biology”. According to the study, the age-related destabilization of the microbiome is not primarily due to changes in the microorganisms themselves, but rather to a decline in immune surveillance. When the aging immune system loses its control function, individual microorganisms can gain the upper hand and disrupt the microbial balance. The study opens new perspectives for understanding healthy aging.
As we age, our cells lose energy and adaptability—a process closely linked to the function of mitochondria, the cell’s “powerhouses”. Researchers at the Leibniz Institute on Aging—Fritz Lipmann Institute (FLI) in Jena have now discovered that the membrane lipid phosphatidylcholine plays a key role in this process. Reduced production of this lipid leads to decline of mitochondrial flexibility and thus contributes significantly to natural mitochondrial aging. However, this process can be influenced by dietary provision of nutrient phosphatidylcholine, which can measurably restore mitochondrial function in aged model organisms. This opens new opportunities for interventions against age-related metabolic decline and for healthy aging.
On November 20, the “10th Long Night of Sciences” will take place in Jena. The FLI will once again actively participate and open its doors to the interested public from 6 p.m. to midnight.