Concomitantly, a reduced ratio of NGF receptors, Tropomyosin receptor kinase A (TrkA—the high-affinity mNGF-specific receptor) to p75 neurotrophin receptor (p75NTR—low-affinity mNGF receptor), has been observed in the basal forebrain during AD progression [7,8,9], further hampering mNGF uptake and altered downstream signaling, leading to cognitive dysfunction [1,10]. This evidence concerns the gene NGFR and Alzheimer disease.