To demonstrate a reduction in synaptic plasticity associated with cognitive decline and due to all these AD hallmarks presented in Gadd45a−/− mice, we evaluated some relevant neurotrophins such as neurotrophin 3 (Nt3), brain-derived neurotrophic factor (Bdnf), nerve growth factor (Ngf), tropomyosin receptor kinase A (TrkA), and tropomyosin receptor kinase B (TrkB) gene expression (Figure 5A–E). This evidence concerns the gene NTRK1 and Alzheimer disease.