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It is noteworthy that although dysregulated microglial function is closely associated with AD pathology—including interactions with Aβ, tau, and emerging processes such as ferroptosis—the hypothesis that microglia-driven neuroinflammation or related ferroptosis serves as an initiating or central driver of human AD still relies predominantly on correlative and preclinical evidence

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Researchers often begin with a larger peptide sequence and then ask a deeper question: Are certain regions of the peptide responsible for specific biological activities