To further address whether AD-relevant mouse models show any skeletal bone deficit and to investigate whether PTH1-34 treatments affect AD-associated bone deficits, we used 5XFAD mouse, a well-characterized AD animal model that expresses mutant human APP and presenilin genes under the control of Thy1-promoter, and exhibit early onset Aβ based brain pathologies (~ 2 MO) and cognition deficits (~ 4 MO) [1, 29, 39]. This evidence concerns the gene APP and Alzheimer disease.