Notably, recent work has shown that noggin overexpression limits tau phosphorylation in human iPSC-derived APOE4 models and, in vivo, rescues phospho-tau deposition and hippocampus-dependent memory in P301S mice [66], suggesting that noggin levels may influence cognition and phospho-tau levels in Alzheimer’s disease and other tauopathies. Here, NOG is linked to early-onset autosomal dominant Alzheimer disease.