This conception is supported by ample lines of evidence: (i) improving spatial memory capabilities and mitigating histopathological alterations, (ii) reducing AD hallmarks (p-Tau and BACE1), (iii) increasing AMP/ATP ratio and p-LKB1 expression which were associated with heightened hippocampal expression of p-AMPK and SIRT1, (iv) modulating autophagic markers; increasing LC3B and Beclin1 while decreasing mTOR, and (v) promoting TFAM expression, a marker for mitochondrial biogenesis. The gene discussed is TFAM; the disease is Alzheimer disease.