Bedsharing in Early Childhood: Frequency, Partner Characteristics, and Relations to Sleep.

Bedsharing (sharing a bed with others during sleep) in early childhood (3-5 years old) is common across Western and non-Western societies alike. Though prior work indicates that bedsharing may relate to impairments in child sleep quantity or quality, the majority of studies conducted in young children are limited to parent-child bedsharing and rely almost exclusively on caregiver reports to measure child sleep. Here, the authors endeavored to gain further insights into the diversity of bedsharing practices among children in the United States, including how different bedsharing partners (caregivers, siblings) might impact actigraphy-derived measures of children's sleep. Using a sample of 631 children ages 2:9 to 5:11 years, we found that over 36% of children bedshared in some form overnight, with approximately 22% bedsharing habitually. In a subset of children for whom actigraphy measures were collected (n = 337), children who bedshared habitually (n = 80) had significantly shorter overnight sleep, later sleep and wake times, and longer naps than solitary sleepers (n = 257), even when controlling for socioeconomic status. Despite supplementing their shorter overnight sleep with longer naps, habitually bedsharing children had significantly shorter 24-hr sleep time than did solitary sleepers, though differences in sleep efficiency were nonsignificant for all sleep periods. Additionally, sleep efficiency, onset latency, and duration did not differ between children who habitually bedshared with siblings versus those who habitually bedshared with parents. The present results add to prior work examining family contextual correlates of sleep differences in early childhood and provide a more objective account of relations between bedsharing and child sleep.

Human and mouse model cognitive phenotypes in Down syndrome: implications for assessment.

The study of cognitive function in Down syndrome (DS) has advanced rapidly in the past decade. Mouse models have generated data regarding the neurological basis for the specific cognitive profile of DS (i.e., deficits in aspects of hippocampal, prefrontal, and cerebellar function) and have uncovered pharmacological treatments with the potential to affect this phenotype. Given this progress, the field is at a juncture in which we require assessments that may effectively translate the findings acquired in mouse models to humans with DS. In this chapter, we describe the cognitive profile of humans with DS and associated mouse models, discussing the ways in which we may merge these findings so as to more fully understand cognitive strengths and weaknesses in this population. New directions for approaches to cognitive assessment in mice and humans are discussed.