Abstract
BackgroundAge-related cognitive deficits negatively affect quality of life and can presage serious neurodegenerative disorders. Despite sleep disruption's well-recognized negative influence on cognition, and its prevalence with age, surprisingly few studies have tested sleep's relationship to cognitive aging.MethodologyWe measured sleep stages in young adult and aged F344 rats during inactive (enhanced sleep) and active (enhanced wake) periods. Animals were behaviorally characterized on the Morris water maze and gene expression profiles of their parietal cortices were taken.Principal FindingsWater maze performance was impaired, and inactive period deep sleep was decreased with age. However, increased deep sleep during the active period was most strongly correlated to maze performance. Transcriptional profiles were strongly associated with behavior and age, and were validated against prior studies. Bioinformatic analysis revealed increased translation and decreased myelin/neuronal pathways.ConclusionsThe F344 rat appears to serve as a reasonable model for some common sleep architecture and cognitive changes seen with age in humans, including the cognitively disrupting influence of active period deep sleep. Microarray analysis suggests that the processes engaged by this sleep are consistent with its function. Thus, active period deep sleep appears temporally misaligned but mechanistically intact, leading to the following: first, aged brain tissue appears capable of generating the slow waves necessary for deep sleep, albeit at a weaker intensity than in young. Second, this activity, presented during the active period, seems disruptive rather than beneficial to cognition. Third, this active period deep sleep may be a cognitively pathologic attempt to recover age-related loss of inactive period deep sleep. Finally, therapeutic strategies aimed at reducing active period deep sleep (e.g., by promoting active period wakefulness and/or inactive period deep sleep) may be highly relevant to cognitive function in the aging community.
Highlights
Age-related cognitive deficits are a highly prevalent and important health risk in the human population, can presage development of age-related neurodegenerative disease [2,3,4], and are a primary reason for elderly placement in assisted living facilities [5]
The F344 rat appears to serve as a reasonable model for some common sleep architecture and cognitive changes seen with age in humans, including the cognitively disrupting influence of active period deep sleep
Therapeutic strategies aimed at reducing active period deep sleep may be highly relevant to cognitive function in the aging community
Summary
Age-related cognitive deficits are a highly prevalent and important health risk in the human population (reviewed in [1]), can presage development of age-related neurodegenerative disease [2,3,4], and are a primary reason for elderly placement in assisted living facilities [5]. Healthy younger adults exposed to experimentally induced selective deprivation of night time (inactive period) deep sleep show some aging-like phenotypes, including daytime sleepiness [14], blood chemistry changes similar to those seen in metabolic syndrome (a potential precursor to the development of type II diabetes) and cognitive deficits [15,16,17]. Recent studies suggest that deep, slow wave sleep during the inactive period promotes memory [18,19,20,21], possibly through localized synaptic [22,23,24] and macromolecular synthesis [25] effects. Despite the seemingly similar effects of age and sleep dysregulation on cognition, and the high prevalence of sleep changes with age, relatively few studies have investigated possible mechanistic links between sleep architecture changes and agerelated cognitive decline. Despite sleep disruption’s well-recognized negative influence on cognition, and its prevalence with age, surprisingly few studies have tested sleep’s relationship to cognitive aging
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