Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the leading cause of dementia worldwide, defined pathologically by extracellular amyloid-β plaques and intraneuronal neurofibrillary tangles composed of hyperphosphorylated tau—lesions that together drive extensive neurodegeneration. Curcumin (CUR), a polyphenol derived from
Curcuma longa
, has attracted considerable interest for its multi-targeted therapeutic profile, exerting antioxidant, anti-amyloid, anti-inflammatory, and anti-tau effects against AD pathology. Its clinical translation, however, has been severely constrained by poor aqueous solubility and inadequate penetration of the blood–brain barrier (BBB). In recent years, nanocarrier systems have emerged as a promising strategy to overcome these delivery barriers. In this review, we critically assess the performance of CUR-loaded polymeric, lipid-based, inorganic, and protein-based/biomimetic nanoformulations in preclinical AD models, with a focus on the mechanisms through which they mitigate Aβ aggregation, tau hyperphosphorylation, neuroinflammation, and oxidative stress. The accumulated preclinical evidence supports the rationale for CUR-based nanomedicines as a multi-targeted therapeutic approach, yet the translational outlook remains guarded: to date, no brain-targeted CUR nanoformulation has entered clinical evaluation, and substantial hurdles, including scalable manufacturing, regulatory qualification, and long-term safety assessment, must be addressed before this approach can meaningfully benefit patients.