Collectively, these results indicate that direct genetic DYRK1A modulation (knockdown or overexpression) in the brain modulates memory performance and various AD-related pathologies including proinflammatory responses, Aβ burden, and tauopathy in 5xFAD, PS19, and/or WT mice implicating DYRK1A as a promising target for AD intervention. This evidence concerns the gene DYRK1A and tauopathy.