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Early initiating events in Alzheimer’s disease (AD) go beyond amyloid pathology. Focusing on the entorhino-hippocampal system, it is shown that microglial activation and neuronal inflammasomes such as NLRP1 and NLRP3 in neuroinflammation in early AD. Evidence is presented on how cytokine polymorphisms, tau oligomerization, and trace element imbalances contribute to disease progression. Recent findings highlight the interplay between tau pathology, inflammasome activation, and blood–brain barrier disruption. Together, these mechanisms suggest that immune dysregulation and altered homeostasis are central to the initiation and propagation of AD.