Previous reports showed that DYRK1A is highly activated in the neocortex, entorhinal cortex, and hippocampus of Alzheimer’s disease (AD) patients7 and can phosphorylate downstream targets, including the amyloid precursor protein (APP) and tau protein, leading to the formation of amyloid β (Aβ) and neurofibrillary tangles (NFTs).8 This evidence concerns the gene APP and early-onset autosomal dominant Alzheimer disease.