For example, the upregulation of casein kinase 1 (CK1) in ALS, FTLD-TDP, and Alzheimer’s disease suggests that enhanced kinase activity may drive the increased phosphorylation of aggregating protein substrates including TDP-43, tau, and α-synuclein [20, 24, 142–144]. This evidence concerns the gene TARDBP and early-onset autosomal dominant Alzheimer disease.