The Resolution Failure: Reframing Alzheimer's Pathology as an Interaction-Completion Deficit

This paper proposes a reframing of Alzheimer’s disease pathology as a failure of immune interaction completion rather than a failure of immune recognition. It argues that beta-amyloid persistence reflects sustained innate immune engagement that does not receive the signals required to terminate, resulting in chronic inflammation and secondary neural damage. The framework separates target identification from response governance, introducing a modular “tag and govern” architecture in which recognition forcing enables immune engagement while resolution biasing enables disengagement and completion. This perspective offers a structural explanation for limitations observed across cholinergic, amyloid-centric, and anti-inflammatory research approaches. This work is conceptual in nature and does not propose experimental protocols or therapeutic claims. It is intended to guide future investigation toward immune interaction completion rather than suppression or symptom modulation. The paper was developed through a symbiotic human–AI reasoning process and is released into the public domain (CC0) to remove institutional, legal, and economic barriers to reuse, testing, or extension.