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The lack of a severe dendritic pathology in Ts65Dn pups is reminiscent of the delayed appearance of patent dendritic alterations in newborns with DS. This suggests that dendritic defects may be related to dendritic compartment and age. This study shows dendritic branching defects that mainly involve the basal domain in P2 Ts65Dn mice and the apical but not the other domains in P8 Ts65Dn mice. No genotype effects were detected on either somatic or dendritic spine density. In P8 Ts65Dn mice, the distalmost apical branches were missing or reduced in number, but there were no alterations in the collateral and basal dendrites. In P2 Ts65Dn mice, we found a moderate hypotrophy of the apical and collateral dendrites but a patent hypotrophy of the basal dendrites. In Golgi-stained brains, we quantified the dendritic arbors of layer II/III pyramidal neurons in the frontal cortex of Ts65Dn mice aged 2 (P2) and 8 (P8) days and their euploid littermates. Thus, the goal of the current study was to establish whether dendritic alterations are already present in the neonatal period in Ts65Dn mice. In contrast, there is scarce information regarding dendritic alterations at early life stages in this and other models, although there is evidence for dendritic alterations in adult mouse models. Neurogenesis alterations across the life span have been extensively studied in the Ts65Dn mouse. While neurogenesis impairment in DS is a fetal event, dendritic pathology occurs after the first postnatal months. These defects are replicated in the Ts65Dn mouse, a widely used model of DS. ID can be ascribed to both neurogenesis impairment and dendritic pathology. Down syndrome (DS), which is due to triplication of chromosome 21, is constantly associated with intellectual disability (ID).