Aging-associated diseases are a major challenge of the contemporary society, and finding ways to improve human healthspan – the time that a person can lead a healthy active life – is one of the primary objectives of biomedical research. It is increasingly understood that biological aging is not a specific genetic program but rather a consequence of “evolutionary neglect”. This is because in nature, animals die primarily due to age-independent causes, such as predation and diseases, and thus there is limited selective pressure to evolve long-lived organisms. As a result, the lifespan of different animal species varies greatly, from weeks in the roundworm C. elegans to several months in the killifish to hundreds of years in whales and sharks and to near immortality in some flatworms and hydra. The fact that very short- and very long-lived animal species do exist suggests that aging is an adjustable process.
Researchers at ERIBA have recently demonstrated that the regeneration-capable flatworm Macrostomum lignano has a surprisingly long lifespan and manifests age-related regulation of numerous genes important for the maintenance of biological quality, including DNA repair, protein homeostasis and stem cell activity. In this project they will use the generated knowledge on ageing in M. lignano to evaluate multiple genes for their potential role as “healthspan boosters” using a pyramid of model organisms, from roundworm Caenorhabditis elegans to short-lived fish Nothobranchius firzeri to mouse. As a result of this project, they expect to identify multiple novel genes and pathways that can be exploited for healthspan extension.