Except for the crucial role of truncated Dyrk1A in AD pathology, autism‐associated truncation mutations of Dyrk1A, R205X, and E239X, cause loss of function and lead to defects in the dendritic outgrowth, dendritic spine density, and cortical migration during neuron development in autism spectrum disorder.55 This evidence concerns the gene DYRK1A and Alzheimer disease.