Effects of sleep deprivation and aging on long-term and remote memory in mice

Vecsey, Christopher G.; Park, Alan J.; Khatib, Nora; Abel, Ted

doi:10.1101/lm.036590.114

Cited by 17 publications

(16 citation statements)

References 72 publications

(73 reference statements)

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“…Acute sleep deprivation and chronic sleep restriction cause significant decrements in short-term and long-term memories in humans and in animal models. [3][4][5][6][7][8][9] In mammals, the consolidation of hippocampal dependent spatial memory is particularly susceptible to the effects of sleep deprivation. [10][11][12] In Drosophila and mouse models, genetic mutants exhibiting reduced sleep also show impairments in memory.…”

Section: Introductionmentioning

confidence: 99%

Acute Sleep Deprivation Blocks Short- and Long-Term Operant Memory inAplysia

Krishnan

Gandour

Ramos

et al. 2016

Sleep

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Study Objectives: Insufficient sleep in individuals appears increasingly common due to the demands of modern work schedules and technology use. Consequently, there is a growing need to understand the interactions between sleep deprivation and memory. The current study determined the effects of acute sleep deprivation on short and long-term associative memory using the marine mollusk Aplysia californica, a relatively simple model system well known for studies of learning and memory. Methods: Aplysia were sleep deprived for 9 hours using context changes and tactile stimulation either prior to or after training for the operant learning paradigm, learning that food is inedible (LFI). The effects of sleep deprivation on short-term (STM) and long-term memory (LTM) were assessed. Results: Acute sleep deprivation prior to LFI training impaired the induction of STM and LTM with persistent effects lasting at least 24 h. Sleep deprivation immediately after training blocked the consolidation of LTM. However, sleep deprivation following the period of molecular consolidation did not affect memory recall. Memory impairments were independent of handling-induced stress, as daytime handled control animals demonstrated no memory deficits. Additional training immediately after sleep deprivation failed to rescue the induction of memory, but additional training alleviated the persistent impairment in memory induction when training occurred 24 h following sleep deprivation. Conclusions: Acute sleep deprivation inhibited the induction and consolidation, but not the recall of memory. These behavioral studies establish Aplysia as an effective model system for studying the interactions between sleep and memory formation.

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Section: Introductionmentioning

confidence: 99%

Acute Sleep Deprivation Blocks Short- and Long-Term Operant Memory inAplysia

Krishnan

Gandour

Ramos

et al. 2016

Sleep

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“…A group of young women (20-30 years) were shown to be more vulnerable to 4 hours of sleep loss for 3 nights compared to older women (55-65 years) when tested by psychomotor vigilance test [72]. In a remarkable parallel, rodent studies have shown that sleep deprivation induced memory loss affects young animals more than the older animals [28]. Greater susceptibility of younger individuals that reflect in worsened neurobehavioral parameters post sleep loss might stem from the fact that young age group needs more sleep compared to older individuals.…”

Section: Metabolomics Studies Of Experimental Sleep Deprivationmentioning

confidence: 99%

“…Other molecular processes related to biological aging such as DNA damage response and cellular senescence was also associated to partial sleep deprivation in humans [27]. On the other hand, neurobehavioral studies on younger and older populations have convincingly shown that young individuals are more affected by loss of sleep from perspectives of attention, cognition and learning and memory [28]. Such observation suggests that older individuals are more resistant to effects of sleep loss while younger ones are vulnerable, even demonstrating signatures of "aging-like" characteristics post sleep loss.…”

Section: Introductionmentioning

confidence: 98%

Metabolism of sleep and aging: Bridging the gap using metabolomics

Sengupta

Weljie

2019

NHA

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Sleep is a conserved behavior across the evolutionary timescale. Almost all known animal species demonstrate sleep or sleep like states. Despite extensive study, the mechanistic aspects of sleep need are not very well characterized. Sleep appears to be needed to generate resources that are utilized during the active stage/wakefulness as well as clearance of waste products that accumulate during wakefulness. From a metabolic perspective, this means sleep is crucial for anabolic activities. Decrease in anabolism and build-up of harmful catabolic waste products is also a hallmark of aging processes. Through this lens, sleep and aging processes are remarkably parallel-for example behavioral studies demonstrate an interaction between sleep and aging. Changes in sleep behavior affect neurocognitive phenotypes important in aging such as learning and memory, although the underlying connections are largely unknown. Here we draw inspiration from the similar metabolic effects of sleep and aging and posit that large scale metabolic phenotyping, commonly known as metabolomics, can shed light to interleaving effects of sleep, aging and progression of diseases related to aging. In this review, data from recent sleep and aging literature using metabolomics as principal molecular phenotyping methods is collated and compared. The present data suggests that metabolic effects of aging and sleep also demonstrate similarities, particularly in lipid metabolism and amino acid metabolism. Some of these changes also overlap with metabolomic data available from clinical studies of Alzheimer's disease. Together, metabolomic technologies show promise in elucidating interleaving effects of sleep, aging and progression of aging disorders at a molecular level. process of aging is in part the result of progressive decline of physiological function at the molecular level. Key physiological processes impacted by aging include genomic instability, telomere attrition, epigenetic alteration, loss of proteastasis, nutrient sensing dysregulation, mitochondrial dysfunction, cellular senescence, stem cell exhaustion and altered intercellular communication [3].Along with molecular level changes, behavioral changes are also apparent with healthy aging. Memory impairment [4] and altered sleep wake activities are perhaps the most common signatures of aged individuals [4]. Both human population and rodent model studies have shown that aging individuals are unable to sustain sleep/wake state and generally

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“…The elderly are less tolerant to SD. It has been shown that SD impairs remote memory in aged mice, with changes in gene expression in the hippocampus [9,10]. SD also has detrimental effects on glucose metabolism outside of the brain in peripheral organs.…”

Section: Sleep Deprivationmentioning

confidence: 99%

The potential use of physical resilience to predict healthy aging

Schorr

Carter

Ladiges

2017

Pathobiology of Aging & Age-related Diseases

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Physical resilience is the ability of an organism to respond to stressors that acutely disrupt normal physiological homeostasis. By definition, resilience decreases with increasing age, while frailty, defined as a decline in tissue function, increases with increasing age. Assessment of resilience could therefore be an informative early paradigm to predict healthy aging compared to frailty, which measures late life dysfunction. Parameters for resilience in the laboratory mouse are not yet well defined, and no single standardized stress test exists. Since aging involves multiple genetic pathways, integrative responses involving multiple tissues, organs, and activities need to be measured to reveal the overall resilience status, suggesting a battery of stress tests, rather than a single all-encompassing one, would be most informative. Three simple, reliable, and inexpensive stressors are described in this review that could be used as a panel to determine levels of resilience. Brief cold water immersion allows a recovery time to normothermia as an indicator of resilience to hypothermia, i.e. the quicker the return to normal body temperature, the more robust the resilience. Sleep deprivation (SD) impairs remote memory in aged mice, and has detrimental effects on glucose metabolism. Cyclophosphamide (CYP) targets white blood cells, especially myeloid cells resulting in neutropenia with a rebound neutrophilia in an age-dependent manner. Thus a strong neutrophilic response indicates resilience. In conclusion, resilience promises to be an especially useful measurement of biological age, i.e. how fast a particular organ or tissue ages. The three stressors, cold, SD, and CYP, are applicable to human medicine and aging because they represent clinically relevant stress conditions that have effects in an age-dependent manner. They are thus an attractive perturbation for resilience testing in mice to measure the effectiveness of interventions that target basic aging processes.

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Effects of sleep deprivation and aging on long-term and remote memory in mice

Cited by 17 publications

References 72 publications

Acute Sleep Deprivation Blocks Short- and Long-Term Operant Memory inAplysia

Acute Sleep Deprivation Blocks Short- and Long-Term Operant Memory inAplysia

Metabolism of sleep and aging: Bridging the gap using metabolomics

The potential use of physical resilience to predict healthy aging

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