Last month the popular press was doing its normal breathless job of failing to adequately understand and present the facts in relation to research into aging and longevity. In this case it related to recent research into hydra. These small water creatures may be ageless, or at least age very slowly, and are certainly very competent when it comes to regeneration from injury, but that's about as far as it goes - it seems unlikely that profound advances immediately applicable to humans lurk in hydra biology. Instead this is the standard slow gathering of new knowledge, adding to the grand picture of the evolution of aging, longevity, and the plethora of individual mechanisms that contribute to these traits.
Here is a short open access commentary on the recent hydra research:
Clues to the role of FOXO3A in controlling longevity may be available through the comparative study of organisms which show no sign of aging. One of the very few examples of animals which appear to be truly immortal is the freshwater polyp Hydra. Much of Hydra's remarkable immortality can be traced back to the asexual mode of reproduction by budding which requires a tissue consisting of stem cells with continuous self-renewal capacity. [Hydra's] stem cells indeed continuously proliferate and generate eternal lineages. How? This question has been plaguing some of us since the late 1980s.
In the new study, a literally immortal model organism was induced to both stem cell senescence and immune senescence by altering the expression level of a single gene, the longevity factor FoxO. The data suggest that FoxO has ancient roles in controlling stem cell behavior that may underlie longevity.
The findings have captured the imagination of the popular press, and raised the skeptic's eyebrows. What lessons can actually be learned from the Hydra study? What does this mean for understanding human longevity? First, the Hydra results have moved the longevity-enabling FOXO3A gene from reported association to possible functions, corroborating and extending beyond previous observations in C. elegans and Drosophila. Second, the link between FoxO and components of the innate immune system is of particular interest since aging processes in humans are known to result in impairment of both innate and adaptive immunity ("immunosenescence") as well as in a pro-inflammatory status ("inflammaging"). Third, the Hydra study strengthens the earlier described role of FOXO3A in human stem cell maintenance and regulation. This hypothesis warrants further investigation and indicates another plausible mechanism through which FOXO3A variation may exert its effect on longevity. Attempts to extend the lessons learnt from Hydra to more complex organisms including humans will be challenging. However, the recent study is a proof of principle that investigations in Hydra stem cells hold promise. The more we learn about the role of FoxO in Hydra, the better we will understand how the gene and its variants contribute to longevity in humans.