To address this question, we generated 5XFAD transgenic mice with heterozygous TrkB knockout (TrkB+/–·5XFAD), and tested the effects of TrkB reduction on AD-like features in this mouse model during an incipient stage that shows only modest amyloid-β (Aβ) pathology and retains normal mnemonic function. This evidence concerns the gene NTRK2 and Alzheimer disease.