Nicholas P. Timms
Submitted: December 2025 : Publish: 18th April 2026
Abstract
The scientific investigation of biological aging has traditionally been divided between molecular-genetic perspectives of informational degradation and systemic-physical models of topological network decline. This paper presents a unified theoretical synthesis bridging these epistemological domains by integrating the Atavistic Genetic Expression Dissociation (AGED) hypothesis with the physics of topological phase transitions in disordered media. We propose that the macroscopic structural entropy observed in the aging neural connectome is fundamentally driven by microscopic phylogenetic regression, wherein cells lose their morphostatic information and revert to ancient, unicellular transcriptional states. These uncoordinated, atavistic cells act as localized structural defects, or “scatterers,” that disrupt global biological signal propagation. This accumulation of scatterers drives the brain from a highly integrated, crystalline state of maximal cognitive efficiency into a disordered, fragmented glassy state. Crucially, this synthesis resolves the anomaly of the brain’s unique resistance to full transcriptional atavism; because post-mitotic neurons cannot fully regress to a proliferative, liquid-like state, they are forced into a rigid topological frustration that culminates in a brittle glass transition. Ultimately, this framework reframes biological aging as a universal spatiotemporal decoherence and suggests that future therapeutic interventions must pivot from mere damage clearance toward topological annealing and the restoration of phylogenetic identity.
