Scientific Overview
A concise, research-facing introduction to the Redox Flavin hypothesis.
Motivation
Neurodegenerative diseases, particularly Alzheimer’s disease, show persistent signatures of mitochondrial dysfunction, redox imbalance, and impaired cellular homeostasis. Conventional interventions often target oxidative damage or attempt to raise redox resources (e.g., antioxidants, riboflavin, NAD⁺ precursors). However, these approaches may not restore the cell’s ability to govern redox balance dynamically.
Hypothesis
Redox Flavin hypothesis: redox imbalance can reflect a loss of intrinsic regulatory competence. A flavin-based regulatory control architecture may re-establish homeostatic redox governance by sensing and correcting deviations in a closed-loop manner.
What “adaptive regulation” means
- Sensing relevant redox signals (e.g., flavin redox states, ROS proxies, NAD⁺/NADH context).
- Decision-making with hysteresis to avoid oscillation and overcorrection.
- Actuation via endogenous programs (e.g., antioxidant response, biogenesis, quality control).
- Shutdown once the system returns to a target range (set-point).