Transient mRNA interventions that adapt
to cellular damage in real-time
Why does human lifespan hit a wall at ~125 years? If aging were just accumulated damage, we would expect either gradual distribution across all species or sharp thresholds in all species. Instead, humans show hard limits while lobsters and certain bats demonstrate negligible senescence. This variation indicates that aging mechanisms are programmable rather than thermodynamically inevitable. Cells retain repair capabilities but lose orchestration across timescales and damage types. Therefore, we are building CellOS: programmable mRNA cocktails that monitor damage biomarkers and deliver repair enzymes only when justified. Because mRNA degrades within 24-48 hours, the system adapts continuously. Our computational models demonstrate substantial lifespan extension when coordination is restored.
We are now validating in model organisms.
Our agent-based models reveal critical thresholds for intervention timing and repair intensity. These computational findings now guide our experimental validation program.
A modular platform that combines damage sensing with coordinated repair delivery. Each component operates independently but responds to shared cellular signals, creating an adaptive intervention system.
The system continuously monitors cells for signs of damage across multiple cellular pathways and molecular systems.
When damage is detected, the system activates specific repair mechanisms at the right intensity for each damage type.
The system adjusts based on how cells respond, increasing intervention when needed and reducing it when damage is under control.
Each therapy uses mRNA that naturally degrades in 24-48 hours. This allows precise temporal control and the ability to stop treatment at any time.
Different people have different damage patterns. The platform designs custom combinations based on individual biomarkers.
Starting with computational models that generate testable predictions, then validating in model organisms before any human application.
Multiple independent mRNA therapies rather than one complex system. Each targets a specific damage type and can be tested and optimized separately.
Computational models show that early intervention dramatically outperforms late intervention. Prevention is more effective than treatment after severe damage.
Aging is not just wear and tear. It is a coordination failure. As damage accumulates, cells lose their ability to orchestrate effective repairs. They either over-respond (inflammation, cancer risk) or under-respond (senescence, dysfunction). Our hypothesis: aging stems from degraded cellular decision-making, not just accumulated damage.
Cells face damage on different timescales: acute stress (minutes to hours), chronic oxidative damage (days to weeks), and accumulated mutations (months to years). Current approaches target one timescale. We are building a system that coordinates responses across all three, matching intervention intensity to damage severity and urgency.
We built agent-based models tracking multiple damage pathways across cellular populations. Through extensive parameter testing across different stress levels and repair capacities, our architecture demonstrated high success rates. Most critically: early aggressive intervention substantially outperformed late conservative approaches.
Unlike permanent genetic modifications, mRNA therapies degrade naturally within 24-48 hours. This enables precise temporal control: deploy repair mechanisms when biomarkers justify intervention, then let them clear when no longer needed. High-risk interventions activate only during crises, fundamentally changing the safety profile compared to permanent gene therapy.
Starting 2026, we will validate these computational predictions in model organisms, testing whether mRNA-delivered repair proteins extend lifespan according to model predictions. Success requires dose-dependent responses matching computational thresholds.
This is highly experimental research at the intersection of computational biology and therapeutic development. We are in early-stage validation with no guarantees of success.
Principal Investigator
Dr. Chudzik directs the Foundation's research on programmable cellular interventions. His background in computational neuroscience and machine learning for brain aging led to a fundamental question: if we can measure cellular decline through digital biomarkers, can we reverse it through intelligent molecular interventions? This question drives the current work on mRNA-based repair systems.
Current research: agent-based models of cellular aging, mRNA therapeutic design for damage-specific repair, and experimental validation in model organisms. The approach tests whether restoring cellular coordination across damage types and timescales can extend functional lifespan.
Head of Product
Katarzyna Malecka brings extensive senior product management experience. She has driven product roadmaps, managed cross-functional teams, and delivered complex technology initiatives from conception through deployment. She holds certifications in PRINCE2, AgilePM, and Scrum methodologies.
At the Foundation, she manages organizational operations, strategic planning, and external partnerships. Her background in stakeholder coordination and governance ensures the Foundation maintains ethical research standards and operational transparency.