Neuroimmune Dysregulation in Early‐Onset Alzheimer's Disease: Astrocyte‐Mediated Innate Immune Hyperactivation Drives Pathogenic Feedforward Loops and Amyloid‐Beta/Tau Pathology

Alzheimer's disease (AD) heterogeneity reflects distinct etiologies: EOAD is characterized by a hyperimmune state driven by astrocytic immune hyperactivity due to genetic susceptibility and environmental triggers, while LOAD arises from an aging-related immunosenescence process. Both pathways ultimately converge on Aβ/tau deposition as secondary outcomes. This paradigm shift highlights the central role of innate immunity in AD pathogenesis, providing novel therapeutic targets to disrupt pathological cycles via immune modulation.