Specifically, after crossing TrkB+/– knockout and 5XFAD transgenic mice, we examined the effects of TrkB haploinsufficiency (that is, 50% reduction) on the development of AD-like phenotypes, including cognitive impairments, Aβ accumulation and aberrant hippocampal signaling pathways, in young 5XFAD mice that show only modest plaque pathology and still retain normal learning and memory function. This evidence concerns the gene NTRK2 and Alzheimer disease.