The above-cited studies of the contribution of overexpressed DYRK1A to brain β-amyloidosis, neurofibrillary degeneration, neuronal loss, and dementia indicate that therapeutic inhibition of excessive activity of overexpressed DYRK1A in DS individuals may disrupt both pathological pathways and arrest/slow down neurodegeneration, neuronal loss, and related functional decline [92]. This evidence concerns the gene DYRK1A and Dravet syndrome.