Subsequent pioneering work by the same research team, showed that both chronic stress and BDNF deficiency significantly inhibit this BDNF-dependent GR phosphorylation, resulting in impairments in memory retention and post-training dendritic spine preservation (68), increased Tau phosphorylation and development of Tau neuropathology (69), as well as exacerbation of the neuropathological manifestations of the APP/PS1 mouse model of AD (70). The gene discussed is NR3C1; the disease is Alzheimer disease.