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AD pathology is now seen as a complex network where insulin signaling issues, A accumulation, and tau hyperphosphorylation interact and worsen each other within the A/T/N framework (Amyloid/Tau/Neurodegeneration) ( 4.3 Impaired glycolytic flux and TCA cycle disruption Extensive research has highlighted the association between AD and the dysregulation of key glycolytic enzymes, including hexokinase, glyceraldehyde 3-phosphate dehydrogenase (GAPDH), and pyruvate kinase (PK) ( 4.4 Altered lipid metabolism and membrane remodeling Beyond glucose impairment, a growing body of epidemiological and clinical evidence links disrupted lipid metabolism to the pathophysiology and progression of AD

Abstract Background Maintaining the structural and functional integrity of the bloodbrain barrier (BBB) is vital for neuronal equilibrium and optimal brain function

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