When integrated, our findings support an AD-relevant mechanism where C. racemosa lipids (i) partially preserve acetylcholine signaling via ACHE/CHRM1 modulation, (ii) reduce oxidative/nitrosative stress through NOS1/NOS2 interaction and antioxidant reinforcement, and (iii) suppress arachidonic-acid and glial inflammatory cascades via PEA/oleamide-linked lipid mediators, collectively yielding a synergistic neuroprotective profile appropriate for the multifactorial pathology of Alzheimer’s disease. The gene discussed is ACHE; the disease is Alzheimer disease.