Less is more? Gene switch for healthy aging found
Ageing is the main risk factor for becoming frail and for developing different ageing-associated diseases, like cancer, heart disease, type II diabetes and Alzheimer. Instead of treating these different diseases separately a main aim in ageing research is to delay the ageing process as a whole and thereby to postpone the emergence of these age-related conditions altogether.
The Calkhoven laboratory at ERIBA and collaborators from the Fritz Lippmann Institute (Jena, Germany) published in eLIfe that mutant mice with reduced production of the transcription factor C/EBPβ-LIP live longer and show signs of delayed ageing. In previous work, they showed that these mutant mice display metabolic improvements similar to those achieved by calorie restriction, a dietary measurement that is famously know to improve health- and lifespan in different species (DOI 10.15252/embr.201439837).
In the new eLife publication Calkhoven and colleagues now show that female mice with the mutation live longer and are less susceptible to cancer development. In addition, as mutant mice age they gained less weight, maintained better motor coordination, can better handle changes in blood glucose and have a more juvenile immune system, compared to control animals.
The study suggests that drugs that target C/EBPβ-LIP could potentially delay ageing and age-related diseases.
The publication can be found here: eLife 2018;7:e34985 DOI: 10.7554/eLife.34985
See also Nature Research Highlight: https://www.nature.com/articles/d41586-018-05125-wBack to previous page