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In this study we demonstrate that, glutamate per se induced synthesis of thrombogenic peptides, plasminogen activator inhibitor-1 and hypoxia-inducible factor-2, from pre-existing mRNAs in enucleate platelets, stimulated cytosolic calcium entry, upregulated RhoA-ROCK-myosin light chain/myosin light chain phosphatase axis, and elicited extensive shedding of extracellular vesicles from platelets

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