Increased pathological aggregates: Experiments in AD mice revealed FSH acts independently of other HPO axis players to bind FSHR in the hippocampus and activate CCAAT/enhancer binding protein β–asparaginyl endopeptidase (C/EBPβ–AEP) to initiate δ-secretase activity, increasing cleavage of APP to its pathological forms. FSH dosing also induced tau phosphorylation and pTau accumulation, as well as amyloid plaque accumulation, and loss of dendritic spines (68). The gene discussed is FSHR; the disease is Alzheimer disease.