DYRK1A and Alzheimer disease: However, kinase specificity of truncated DYRK1A is reduced leading to increase its affinity toward STAT3α, a major regulator of inflammation We demonstrate that decreasing production of DYRK1A truncated forms by Leucettine L41 in an AD-like mouse model, reduces levels of inflammatory cytokines, improves clearance of amyloid-β plaques through microglia recruitment and activation, and consequently improves synaptic plasticity and memory.