From this perspective, recent evidence implicates DYRK1A as a promising target for AD as it has been associated with both tau and amyloid neuropathologies through DYRK1A-mediated phosphorylation of key substrates: tau, amyloid precursor protein (APP), Neprilysin (NEP), and Presenilin 1 (PSEN1) and SEPT4 (Table 1). This evidence concerns the gene MME and amyloidosis.