Chronic Caffeine Treatment Prevents Sleep Deprivation-Induced Impairment of Cognitive Function and Synaptic Plasticity

Alhaider, Ibrahim A.; Aleisa, Abdulaziz M.; Tran, Trinh T.; Alzoubi, Karem H.; Alkadhi, Karim A.

doi:10.1093/sleep/33.4.437

Cited by 131 publications

(109 citation statements)

References 59 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Hippocampal-dependent learning was assessed using the Mnemonic Similarity Task (Fig. 1B) (Kirwan and Stark, 2007;Yassa et al, 2011;, a validated paradigm sensitive to hippocampal subfield function in humans, particularly pattern separation in the CA3/DG subfield. All task sessions were presented using the Psychtoolbox toolkit within MATLAB (The MathWorks), with task versions (each with unique stimuli) used in a counterbalanced order across the three experimental conditions (rested, deprivation, recovery).…”

Section: Methodsmentioning

confidence: 99%

“…The Mnemonic Similarity Task allows for the concurrent assessment of two learning measures: the Lure Discrimination Index (LDI or "separation bias") (Kirwan and Stark, 2007; and Recognition Memory Accuracy, with LDI demonstrating greater dependence upon the hippocampus (Brock Kirwan et al, 2012), and specifically the CA3/DG subfield region in particular (Kirwan and Stark, 2007;Bakker et al, 2008;Tamminga et al, 2010;Lacy et al, 2011). LDI is defined as the difference between the proportion of lure items correctly identified as "similar" and the proportion of newly presented foil images incorrectly identified as "similar."…”

Section: Methodsmentioning

confidence: 99%

“…Second, sleep deprivation impairs the necessary molecular and cellular mechanisms underlying neuronal plasticity expressed within these hippocampal subregions . Third, NREM slow waves and sleep spindles, the cardinal features of the NREM electroencephalogram (EEG), positively predict next-day hippocampus-dependent learning under sleeprested conditions, representing candidate oscillations that may additionally restore hippocampal function following sleep deprivation (Mander et al, 2011;Antonenko et al, 2013). Fourth, these same oscillations increase in a homeostatic manner following sleep deprivation (Dijk et al, 1993), potentially indexing a use-dependent recovery mechanism for neural plasticity that may restore hippocampal functioning following sleep loss (Walsh et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Human Hippocampal Structure: A Novel Biomarker Predicting Mnemonic Vulnerability to, and Recovery from, Sleep Deprivation

et al. 2016

View full text Add to dashboard Cite

Sleep deprivation impairs the formation of new memories. However, marked interindividual variability exists in the degree to which sleep loss compromises learning, the mechanistic reasons for which are unclear. Furthermore, which physiological sleep processes restore learning ability following sleep deprivation are similarly unknown. Here, we demonstrate that the structural morphology of human hippocampal subfields represents one factor determining vulnerability (and conversely, resilience) to the impact of sleep deprivation on memory formation. Moreover, this same measure of brain morphology was further associated with the quality of nonrapid eye movement slow wave oscillations during recovery sleep, and by way of such activity, determined the success of memory restoration. Such findings provide a novel human biomarker of cognitive susceptibility to, and recovery from, sleep deprivation. Moreover, this metric may be of special predictive utility for professions in which memory function is paramount yet insufficient sleep is pervasive (e.g., aviation, military, and medicine).

show abstract

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Human Hippocampal Structure: A Novel Biomarker Predicting Mnemonic Vulnerability to, and Recovery from, Sleep Deprivation

et al. 2016

View full text Add to dashboard Cite

show abstract

“…Caffeine enhances alertness by antagonism of adenosine A1 receptor and increases cAMP signaling through inhibition of phosphodiesterase (Fredholm et al 1999;Wu et al 2009). Chronic caffeine administration has been shown to prevent sleep loss-induced impairment of cognitive function and synaptic plasticity (Alhaider et al 2010b). Another stimulant, modafinil, prescribed for treatment of excessive daytime sleepiness, prevents sleep-deprivation induced cognitive impairments (Moreira et al 2010).…”

Section: Resultsmentioning

confidence: 99%

The impact of sleep loss on hippocampal function

2013

View full text Add to dashboard Cite

Hippocampal cellular and molecular processes critical for memory consolidation are affected by the amount and quality of sleep attained. Questions remain with regard to how sleep enhances memory, what parameters of sleep after learning are optimal for memory consolidation, and what underlying hippocampal molecular players are targeted by sleep deprivation to impair memory consolidation and plasticity. In this review, we address these topics with a focus on the detrimental effects of post-learning sleep deprivation on memory consolidation. Obtaining adequate sleep is challenging in a society that values "work around the clock." Therefore, the development of interventions to combat the negative cognitive effects of sleep deprivation is key. However, there are a limited number of therapeutics that are able to enhance cognition in the face of insufficient sleep. The identification of molecular pathways implicated in the deleterious effects of sleep deprivation on memory could potentially yield new targets for the development of more effective drugs.

show abstract

“…In the context of sleep perturbations and learning, most studies have reported on the presence of cognitive impairments with sleep deprivation by exploring a large array of learning and memory tests including the radial arm maze (44,45), Morris water maze (6,46), contextual fear conditioning (47), and eight-box task (48). However, there is only a paucity of cognitive studies exploring the effects of SF, and those were restricted to short-term SF, the latter using methodologies that were associated with substantial alterations in sleep architecture (4)(5)(6).…”

Section: Discussionmentioning

confidence: 99%

Sleep Fragmentation Induces Cognitive Deficits Via Nicotinamide Adenine Dinucleotide Phosphate Oxidase–dependent Pathways in Mouse

Nair

Zhang

Ramesh

et al. 2011

Am J Respir Crit Care Med

158

133

View full text Add to dashboard Cite

Rationale: Sleep fragmentation (SF) is one of the major characteristics of sleep apnea, and has been implicated in its morbid consequences, which encompass excessive daytime sleepiness and neurocognitive impairments. We hypothesized that absence of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity is neuroprotective in SF-induced cognitive impairments. Objectives: To examine whether increased NADPH oxidase activity may play a role in SF-induced central nervous system dysfunction. Methods: The effect of chronic SF during the sleep-predominant period on sleep architecture, sleep latency, spatial memory, and oxidative stress parameters was assessed in mice lacking NADPH oxidase activity (gp91phox-/Y ) and wild-type littermates. Measurements and Main Results: SF for 15 days was not associated with differences in sleep duration, sleep state distribution, or sleep latency in both gp91phox-/Y and control mice. However, on a standard place training task, gp91phox-/Y mice displayed normal learning and were protected from the spatial learning deficits observed in wildtype littermates exposed to SF. Moreover, anxiety levels were increased in wild-type mice exposed to SF, whereas no changes emerged in gp91phox-/Y mice. Additionally, wild-type mice, but not gp91phox-/Y mice, had significantly elevated NADPH oxidase gene expression and activity, and in malondialdehyde and 8-oxo-29-deoxyguanosine levels in cortical and hippocampal lysates after SF exposures. Conclusions: This work substantiates an important role for NADPH oxidase in hippocampal memory impairments induced by SF, modeling sleep apnea. Targeting NADPH oxidase, therefore, is expected to minimize hippocampal impairments from both intermittent hypoxia and SF associated with the disease. Keywords: NADPH oxidase; sleep fragmentation; neurocognitive impairmentsThe manifestations of obstructive sleep apnea (OSA) reflect the interactions of intermittent hypoxia (IH), intermittent hypercapnia, increased intrathoracic pressure swings, and sleep fragmentation (SF) as elicited by the episodic changes in upper airway resistance during sleep. SF is a common phenomenon among several clinical disorders, and can lead to impaired cognitive function via mechanisms that remain poorly understood (1). Indeed, uninterrupted sleep for a minimum length of time is required for optimal daytime vigilance and neurocognitive function (1-3). Preliminary studies in rodents using short-term SF paradigms have also confirmed the adverse effects of SF on learning and seem to be independent of adenosine-mediated synaptic inhibition (4-7).In clinical populations with severe SF (e.g., in OSA) total sleep time typically diminishes only slightly (8). The effects of experimentally induced SF on sleep patterns have not been critically characterized in rodents. It is likely that OSA-induced sleep perturbations are accompanied by obvious cognitive deficits because of increased levels of systemic markers of oxidative stress and inflammation, the latter leading to gray matter loss in neural...

show abstract

Chronic Caffeine Treatment Prevents Sleep Deprivation-Induced Impairment of Cognitive Function and Synaptic Plasticity

Abstract: The results suggest that long-term use of a low dose of caffeine prevents impairment of short-term memory and E-LTP in acutely sleep-deprived rats.

Cited by 131 publications

References 59 publications

Human Hippocampal Structure: A Novel Biomarker Predicting Mnemonic Vulnerability to, and Recovery from, Sleep Deprivation

Human Hippocampal Structure: A Novel Biomarker Predicting Mnemonic Vulnerability to, and Recovery from, Sleep Deprivation

The impact of sleep loss on hippocampal function

Sleep Fragmentation Induces Cognitive Deficits Via Nicotinamide Adenine Dinucleotide Phosphate Oxidase–dependent Pathways in Mouse

Contact Info

Product

Resources

About