ARC-18, a synthetic derivative of the plant compound arctigenin, demonstrated dual mechanisms against Alzheimer's pathology in transgenic mice. After three months of oral treatment, 5×FAD mice showed improved performance in water maze and object recognition tasks, alongside reduced amyloid-beta accumulation in hippocampus and cortex regions. The compound operates through adiponectin receptor 1 (AdipoR1) activation, triggering cellular autophagy that clears protein aggregates while simultaneously reducing BACE1 enzyme activity to limit new amyloid production. This dual-pathway approach represents a sophisticated strategy addressing both amyloid clearance and production—a combination that has proven challenging in previous Alzheimer's interventions. The AdipoR1 target is particularly intriguing given adiponectin's established roles in metabolic health and neuroinflammation. While the cognitive improvements in this mouse model are encouraging, the compound's bioavailability, safety profile, and efficacy in human subjects remain unestablished. The three-month treatment duration, though substantial for rodent studies, represents a fraction of the decades-long disease progression in humans. Most significantly, this work adds to mounting evidence that autophagy enhancement may offer therapeutic value beyond traditional amyloid-targeting approaches that have largely failed in clinical trials.