Disrupting GR phosphorylation at the BDNF-dependent sites Ser134 and Ser267 in an APP/PS1 mouse model with an early-phase AD-like progression aggravated the deleterious effects of the APP/PS1 genotype on mortality, neuroplasticity, and cognition, without affecting amyloid-β deposition or vascular pathology [40]. Here, NR3C1 is linked to Alzheimer disease.