Data from: Sex specific emergence of trisomic Dyrk1a-related skeletal phenotypes in the development of a Down syndrome mouse model

Skeletal insufficiency affects all individuals with Down syndrome (DS) or
Trisomy 21 (Ts21) and may alter bone strength throughout development due
to a reduced period of bone formation and early attainment of peak bone
mass compared to typically developing individuals. Appendicular skeletal
deficits also appear in males before females with DS. In femurs of male
Ts65Dn DS model mice, cortical deficits were pronounced throughout
development, but trabecular deficits and Dyrk1a overexpression were
transitory until postnatal day (P) 30 when there were persistent
trabecular and cortical deficits and Dyrk1a was trending overexpression.
Correction of DS-related skeletal deficits by a purported DYRK1A inhibitor
or through genetic means beginning at P21 was not effective at P30, but
germline normalization of Dyrk1a improved male bone structure by P36.
Trabecular and cortical deficits in female Ts65Dn mice were evident at P30
but subsided by P36, typifying periodic developmental skeletal
normalizations that progressed to more prominent bone deficiencies.
Sex-dependent differences in skeletal deficits with a delayed impact of
trisomic Dyrk1a are important to find temporally specific treatment
periods for bone and other phenotypes associated with Ts21.