Does a healthy lifestyle promote cognitive performance in old age? What new therapeutic approaches can be used to extend the health span in old age? What must the environment look like so that people can age healthy and satisfied? These are just a few examples of the pressing questions that society and politics are currently posing to science. The Leibniz Research Alliance Healthy Ageing wants to provide answers.

  1. Less is more? Gene switch for healthy aging found
    05/28/2018 · FLI Leibniz Institute on Aging - Fritz Lipmann Institute

    Aging is associated with an increase in frailty and age related-diseases. A calorie-restricted diet is known to alleviate these age-related conditions. Researchers from the European Research Institute for the Biology of Ageing (ERIBA) in Groningen, Netherlands, and the Leibniz Institute on Aging – Fritz Lipmann Institute (FLI) in Jena, Germany, now demonstrate in a mouse model that the C/EBPß-LIP gene regulator is involved in the aging process. If LIP is missing, the lifespan of mice increases and the physical fitness is maintained during aging without exposing the mice to a calorie-restricted diet. The research results were published in the renowned journal eLife.

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  2. Surviving in starvation - New mechanism for cell preservation discovered
    05/15/2018 · FLI Leibniz Institute on Aging - Fritz Lipmann Institute

    Scientists from the Leibniz Institute on Aging – Fritz Lipmann Institute (FLI) in cooperation with the Massachusetts Institute of Technology (MIT), Cambridge, Massachusetts, USA, discovered a new mechanism that is important for cells to survive starvation. The protein NUFIP1, which normally occurs in the cell nucleus, migrates into the cytoplasm when there is a lack of nutrients and binds to ribosomes, which are then marked for degradation; an important survival strategy of the cell to ensure the maintenance of the cell upon starvation. The research results were now published in the renowned journal Science.

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  3. Back to sleep: How SETD1A takes blood stem cells to rest
    05/08/2018 · FLI Leibniz Institute on Aging - Fritz Lipmann Institute

    In old age, humans increasingly suffer from infections. In such a case, blood stem cells that are usually inactive are activated in order to produce as many blood and immune cells as needed to fight the infection. However, every cell division entails the risk of accumulating DNA damages, which subsequently can prevent stem cells to become inactive again. Damaged cells are usually detected and eliminated, but if all stem cells are gone, there will be no more reservoir feeding into the mature immune cell pool to defend the body during the next infection. Now, researchers from Leibniz Institute on Aging (FLI) in Jena, Germany, have identified a central mechanism related to the enzyme SETD1A, which is responsible for detecting and repairing DNA damages in blood stem cells and, hence, is crucial for blood stem cells go back to sleep after infections.

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