“…These genetic alterations do not fully represent Down syndrome’s aneuploidy and other mouse and rat models have been developed recently that more faithfully represent the trisomic nature of DS (Kazuki et al, 2020; Kazuki et al, 2022). However, in this study we used the Ts65Dn mouse model because it recapitulates the main skeletal, brain, cognitive, brain metabolite, and genetic alterations associated with DS (Blazek et al, 2011; Costa et al, 2010; Dierssen et al, 2002; Escorihuela et al, 1998; Gupta et al, 2016; Huang et al, 2000; Llambrich, González, et al, 2022; Même, 2014; Starbuck et al, 2021); and the effects of GTE-EGCG pharmacological modulation have been extensively evaluated using this mouse model (Catuara-Solarz et al, 2016; Goodlett et al, 2020; Jamal et al, 2022; Llambrich, González, et al, 2022; McElyea et al, 2016; Stagni et al, 2016; Starbuck et al, 2021; Stringer et al, 2017).…”