# Glymphatic Clearance Hypothesis

Brain fluid transport is real and context dependent; its sleep-specific contribution to ordinary human neurodegeneration remains incompletely established.

Overall Γ follows the registered SC3 clinical disease link, while narrow transport SC1–SC2 retain Ε under an explicit physiological rubric-fit adaptation. Mouse disease perturbations strengthen plausibility and mapped context, but artificial proteinopathy/injury and AQP4's multiple functions restrict human inference. Independent human clinical mediation remains uncrossed. This does not erase the causal transport results or the genuine contradictory measurements.

Measured boundaries include solute size, input pressure, anatomical compartment, anesthesia, circadian phase, microarchitecture, genotype, injury and disease stage. They are defined independently of response. A mapped restricted transport effect is not a universal natural-sleep or human-disease effect.