BUFFALO, NY — April 27, 2026 — A new #hypothesis paper was #published in Volume 18 of Aging-US on April 8, 2026, titled “From Hydra to rotifer and beyond: implications for human aging and delayed senescence.”

The study was led by first and corresponding author Michael Bordonaro from the Geisinger College of Health Sciences. In this work, the author explores a bold and testable hypothesis centered on two very different invertebrate models of aging: the freshwater cnidarian Hydra and the rotifer Brachionus manjavacas. Hydra are well known for their remarkable ability to maintain tissue integrity over time through continuous stem cell renewal, effectively avoiding many of the hallmarks of aging under laboratory conditions. In contrast, rotifers represent the opposite end of the biological spectrum, with short lifespans, fixed somatic cell numbers, and a predictable pattern of age-related decline.

Building on these contrasts, the paper proposes that introducing Hydra-like gene expression patterns into rotifers could delay senescence and extend healthspan. The hypothesis focuses in particular on conserved molecular pathways, including the transcription factor FoxO, which plays a central role in maintaining stem cell function and cellular resilience. Rather than attempting to recreate full stem cell renewal in rotifers—an organism with a fixed adult cell number—the proposed strategy emphasizes improving cellular maintenance, stress resistance, and proteostasis within existing cells.

The paper outlines an iterative experimental framework, beginning with targeted genetic manipulation in rotifers and extending to more complex organisms such as Daphnia and mouse models. This stepwise approach is designed to identify which elements of the Hydra genetic program are truly responsible for its resistance to aging, while also allowing researchers to monitor potential trade-offs, including increased risk of uncontrolled cell growth.

“We hypothesize that delayed senescence at the organismal level is possible through recapitulation of Hydra-like patterns of gene expression in rotifers, and that data obtained may help generate hypotheses for somatic interventions and prioritize pathways for mammalian validation in future studies.”

Importantly, the author emphasizes that complete elimination of aging is unlikely in complex organisms due to evolutionary and biological constraints. Instead, the goal is more realistic: extending healthspan and delaying the onset of age-related decline. The paper also highlights the importance of balancing potential benefits with risks, particularly the possibility that enhancing cellular renewal pathways could increase susceptibility to neoplasia.

Overall, this study presents a conceptual and experimental roadmap for translating insights from simple organisms into strategies that may eventually inform human aging research. By bridging the gap between negligible senescence and rapid aging models, the work provides a fresh perspective on how conserved biological mechanisms might be harnessed to improve health across the lifespan.

DOI - https://doi.org/10.18632/aging.206370

Corresponding author - Michael Bordonaro - [email protected]

Abstract video - https://www.youtube.com/watch?v=YGzYf3W5jNA

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