The purpose of the study was to determine whether fisetin could reduce AD-associated learning and memory deficits and to see how these actions correlated with its effects on AD-related processes implicated in disease progression including amyloid burden, gliosis, oxidative damage, inflammatory pathways and their eicosanoid products as well as dysregulation of the cyclin-dependent kinase 5 (Cdk5) activator p35. This evidence concerns the gene CDK5 and Alzheimer disease.