Notably, it has been used to inhibit the protein 1 (Sp1), a transcription factor involved in AD pathogenesis, while reducing the formation of Aβ and tau hyperphosphorylation, thereby improving cognitive functions.[136, 137] Moreover, after treating APP YAC transgenic mice with tolfenamic acid, the expression of tau and CDK5 was reduced, leading to less phosphorylated tau at sites S235 and T181.[138] Although the precise molecular mechanism by which tolfenamic acid induces Sp1 degradation remains unclear, its impact on AD pathology is remarkable. This evidence concerns the gene CDK5 and Alzheimer disease.