<i>In vitro</i>, OA modulated ACC2 activity through protein kinase A (PKA) signaling, increased fatty acid β-oxidation, reduced lipid droplet accumulation, restored mitochondrial membrane potential and ATP production, and enhanced astrocyte-mediated support of neuronal synaptic growth.<h4>Conclusion</h4>OA ameliorates AD-related pathology and cognitive impairment by restoring astrocytic fatty acid β-oxidation through the PKA/ACACB/CPT1A pathway. This evidence concerns the gene CPT1A and Alzheimer disease.