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All TPP-dependent enzymes contain a highly similar TPP-binding domain and its lack in the TKTL1 encoded protein strongly suggests that it is unlikely that TKTL1 is a TPP-dependent protein capable of catalyzing the transketolase reaction

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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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