Numerous research and development initiatives have emerged from the heterochronic parabiosis studies of the past decade or more, in which an old and a young mouse have their circulatory systems linked. Researchers have moved on from the initial experiments to the search for circulating factors in blood that change in ways that are harmful in aged individuals, and which might be adjusted to improve cell and tissue function. This area of research is one of many to explore the question of how much of degenerative aging is the result of (a) direct consequences of molecular damage versus (b) the result of inappropriate cellular reactions to the existence of damage, the latter mediated to some unknown degree by signaling carried in the bloodstream.

Is it possible to ignore the damage and extend healthy life just by suppressing the reactions to damage? It would be very strange if the answer were that this works comprehensively and damage never has to be repaired. Further, the consequences of any given form of underlying damage can be thought of as a network of diverse chains of cause and effect spreading from a single root: it will require far more work to identify and address all of these reactions to damage than to focus down on a means of repairing the damage. Still, and unfortunately, the concept of damage repair, striking at the root of aging, remains a comparatively unpopular strategy in the research community for some reason. Near all work on the treatment of aging is focused on tinkering with the downstream consequences of damage, and therefore probably a highly inefficient use of funds and time, even given the successes that arise.

One of the more noted scientific teams involved in parabiosis research here report on their recent work, opening this open access paper with a bold statement on the degree to which they believe aging to result from signaling changes, reactions to damage. They are focusing down on just a few signaling factors in the bloodstream, TGF-β and oxytocin, and finding ways to alter amounts in circulation in comparative isolation, without adjusting other factors as well. Given that earlier work on GDF-11 as circulating signal involved in cellular responses to aging has resulted in a great deal of ongoing research and at least one biotech startup, the results here seem interesting enough to drawn in funding for further, similar projects.

Rejuvenation of brain, liver and muscle by simultaneous pharmacological modulation of two signaling determinants, that change in opposite directions with age