NLK and Alzheimer disease: Specifically, Nlk-mediated phosphorylation of Nurr1 is essential for the prevention of neuroinflammation by inhibiting neurotoxic gene expression in microglia via the recruitment of CoREST/lysine-specific demethylase 1 (LSD1) complex for the transrepression of NF-κB activity (44), and mice lacking the histone demethylase Lsd1 display behavioral, neuropathological, and molecular phenotypes that highly overlap with those seen in human AD and FTLD-PGRN cases (45).