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This review integrates current evidence on how brain peptides contribute to AD pathophysiology, summarizes recent progress in peptide-based therapeutic strategies and delivery platforms, and critically examines the remaining barriers to clinical translation, including bloodbrain barrier penetration, metabolic stability, off-target effects, and the need for biomarker-guided patient stratification

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Notably, GGCT knockdown markedly altered mitochondrial morphology and impaired oxidative phosphorylation and glycolysis capacity

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Research demonstrates that copper-binding peptides including GHK-Cu suppress the NF-B pathway through direct molecular interactions, with nuclear translocation of NF-B p65 decreased by approximately 30% upon treatment and molecular modeling showing specific peptide sequences exhibit high binding affinity to NF-B p65 (up to -8.8 kcal/mol)