Alzheimers Disease Progressive Semantic Uncoupling v2.2

Contemporary neurobiology conceptualizes Alzheimer’s disease primarily as a progressive proteinopathy defined by amyloid-β plaques and tau neurofibrillary tangles. While this paradigm catalogs tissue destruction with high resolution, it leaves the clinical structure–function disconnect under-specified: the persistence of intact cognition despite heavy plaque burden, and the rapid narrative fragmentation that often outpaces histological cell loss. This monograph formalizes Alzheimer’s disease as Portal I (Progressive Semantic Uncoupling) within the Informational Nosology framework. Under converging allostatic and syntactic loads, the system enters a compensatory hyperactivation trap that temporarily preserves cognitive output at an unsustainable thermodynamic cost. Concurrently, fragmentation of slow-wave sleep impairs glymphatic clearance, violating the classical macroscopic form of Landauer’s erasure principle and initiating an irreversible proteopathic debt ratchet. Prion-like tau propagation then selectively disconnects Default Mode Network hubs, collapsing cross-frequency phase-locking required for autobiographical continuity. Using an adapted six-variable dynamical skeleton, we show that clinical dementia marks the asymptotic collapse of Causal Conductivity (κ_Ψ → 0) Тhe causal opacity of an uncoupled physical substrate—rather than the literal erasure of stored memory traces. The framework resolves the structure–function paradox and situates Alzheimer’s disease as the canonical gradual portal of high-order semantic constraint failure.