Neural Consequences of Chronic Short Sleep: Reversible or Lasting?

Abstract

Approximately one-third of adolescents and adults in developed countries regularly experience insufficient sleep across the school and/or work week interspersed with weekend catch up sleep. This common practice of weekend recovery sleep reduces subjective sleepiness, yet recent studies demonstrate that one weekend of recovery sleep may not be sufficient in all persons to fully reverse all neurobehavioral impairments observed with chronic sleep loss, particularly vigilance. Moreover, recent studies in animal models demonstrate persistent injury to and loss of specific neuron types in response to chronic short sleep (CSS) with lasting effects on sleep/wake patterns. Here, we provide a comprehensive review of the effects of chronic sleep disruption on neurobehavioral performance and injury to neurons, astrocytes, microglia, and oligodendrocytes and discuss what is known and what is not yet established for reversibility of neural injury. Recent neurobehavioral findings in humans are integrated with animal model research examining long-term consequences of sleep loss on neurobehavioral performance, brain development, neurogenesis, neurodegeneration, and connectivity. While it is now clear that recovery of vigilance following short sleep requires longer than one weekend, less is known of the impact of CSS on cognitive function, mood, and brain health long term. From work performed in animal models, CSS in the young adult and short-term sleep loss in critical developmental windows can have lasting detrimental effects on neurobehavioral performance.

Concise Review: Regulatory Influence of Sleep and Epigenetics on Adult Hippocampal Neurogenesis and Cognitive and Emotional Function

“…Neuroimaging studies show that acute sleep deprivation reduces learning‐related activity in the hippocampus and functional coupling between the hippocampus and cortical regions , consistent with the hypothesis that sleep promotes system‐level memory consolidation by promoting interactions between the hippocampus and cortex . Moreover, after several consecutive days of insufficient sleep, cognitive deficits exhibit a protracted course of recovery, with normal function not observed until after 3 or more nights of recuperative sleep . Thus, the sleep disruptions often experienced by healthy aged individuals as well as patients with Alzheimer's disease have been proposed to contribute to declines in hippocampal‐dependent cognitive function .…”

Caffeine-induced Plasticity of Grey Matter Volume in Healthy Brains: A placebo-controlled multimodal within-subject study

“…Disturbed sleep homeostasis can not only lead to cerebral micromorphometric alterations in the mitochondria and chromatin that leads to cell death [18][19][20] , but also macrostructural changes. Lower GM volumes were observed during abnormally high sleep pressure, such as during sleep deprivation or sleep fragmentation.…”

Cholinergic basal forebrain degeneration due to obstructive sleep apnoea increases Alzheimer’s pathology in mice

“…Lesioned mice had an equivalent number of sleep bouts to control mice (Fig 2D) but had shorter sleep bout, significantly less total sleep and were more active during the sleep phase (Fig 2E,F,G), indicative of disrupted sleep. To further assess the sleep quality in the mice, a 3 hour dim light pulse (30 lux) was applied during the dark (awake) phase on day 3 to induce sleep (Zhao et al, 2017). The lesioned mice also displayed a sleep debt, showing a greater tendency to sleep during a low light period during their active phase on day 3 (Fig 2H,I).…”