Immune Modulation in Alzheimer's Disease via Allergy-Cascade Activation

Alzheimer’s disease is increasingly recognized as a disorder of chronic, maladaptive neuroinflammation driven by persistent microglial activation, Th1/Th17 immune polarization, and blood–brain barrier dysfunction. Therapeutic strategies targeting amyloid-β or tau alone have yielded limited clinical success, suggesting that downstream immune dysregulation plays a central role in disease progression. This review proposes a theoretical immunotherapeutic framework in which the Alleamit™ Immune Modulation Platform leverages-controlled activation of the allergy cascade to redirect immune polarity from neurotoxic Th1/Th17 pathways toward reparative Th2 and regulatory immune states. Recent breakthroughs in protein structure prediction enable the design of highly specific antigens, enabling patient-specific allergens to be engineered based on individual biomarker profiles while minimizing autoimmune risk. The review outlines how immunoglobulin-E-mediated mast cell activation, Th2 cytokine signaling (IL-4, IL-13), and Treg induction may promote microglial repolarization, enhance amyloid clearance, and suppress neuroinflammatory feedback loops. This speculative framework integrates established immunology and neuroinflammation biology with advances in computational protein folding to present a testable hypothesis for personalized immune redirection in Alzheimer’s Disease.