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Abstract Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by extracellular deposition of amyloid-β (Aβ), intracellular hyperphosphorylation of microtubule-associated protein tau and chronic neuroinflammation. At present, effective disease-modifying therapies for AD remain limited. Dexmedetomidine (Dex), a highly selective α2-adrenergic receptor agonist, has been reported in recent years to exert significant neuroprotective effects.
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