Poor Sleep as a Precursor to Cognitive Decline in Down Syndrome : A Hypothesis
On World Down Syndrome Day I want to highlight a well-known and natural treatment for cognitive / behavioral problems. - JR
Poor Sleep as a Precursor to Cognitive Decline in Down Syndrome : A Hypothesis.
Author information
- 1Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
- 2Department of Psychology and Cognitive Science Program, Sonoran University, Center for Excellence in Developmental Disabilities, University of Arizona, Tucson, AZ 85721, USA.
Trisomy for human chromosome 21 (Hsa21; Down syndrome, DS) results in a unique trajectory of developmental outcomes for the brain and craniofacial skeleton. In those with DS, the brain’s overall complexity is reduced owing to fewer cells and narrowing within the sulci and gyri that form its outer contour [1, 2]. Local and interregional connectivity may be altered due to weaker insulation of long-range projections by myelin [3–6], and to differences in how synapses and dendrites mature in response to behavioral experience [7, 8]. Infants with DS exhibit smaller neurocraniums at birth and altogether different morphometric relationships between individual bones of the craniofacial skeleton [9]. These divergent craniofacial features impact breathing [10]. Specifically, tissue crowding produced by midface hypoplasia and realigned soft tissue (i.e., constriction of the pharynx and palate, posterior displacement of the tongue, enlarged tonsilsadenoids) curtails airflow through the upper respiratory tract [11–17]. Propensity toward obesity and reduced muscle tone put further strains on the upper airways [18]. As a result of these medical issues, virtually all people with DS will present symptoms associated with obstructive sleep apnea syndrome (OSAS) and sleep fragmentation [18–24]. The loss of sleep quality wrought by OSAS is predicted to contribute to at least some of the everyday intellectual difficulties experienced by people with DS, presenting a case study in how developmental pathways affected by an extra copy of Hsa21 interact at a macro-level to influence cognitive outcomes later in life.
In this review, we discuss recent evidence linking sleep disruption to Alzheimer disease (AD) and cognitive decline in the typical non-DS population, and stipulate that DS is a population in which these elements might converge. Given the high prevalence of OSAS and AD in DS, we propose that sleep disruption could predispose individuals with DS to earlier onset or faster deterioration with dementia. These factors may be inextricably connected to the DS phenotype-to the extent that all future studies on cognitive development from infancy or cognitive decline in DS must take problematic sleep into account.
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