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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

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10.1038/nchembio.1913