Sleep can improve the off-line memory consolidation of new items of declarative and non-declarative information in healthy subjects, whereas acute sleep loss, as well as sleep restriction and fragmentation, impair consolidation. This suggests that, by modifying the amount and/or architecture of sleep, chronic sleep disorders may also lead to a lower gain in off-line consolidation, which in turn may be responsible for the varying levels of impaired performance at memory tasks usually observed in sleep-disordered patients. The experimental studies conducted to date have shown specific impairments of sleep-dependent consolidation overall for verbal and visual declarative information in patients with primary insomnia, for verbal declarative information in patients with obstructive sleep apnoeas, and for visual procedural skills in patients with narcolepsy-cataplexy. These findings corroborate the hypothesis that impaired consolidation is a consequence of the chronically altered organization of sleep. Moreover, they raise several novel questions as to: a) the reversibility of consolidation impairment in the case of effective treatment, b) the possible negative influence of altered prior sleep also on the encoding of new information, and c) the relationships between altered sleep and memory impairment in patients with other (medical, psychiatric or neurological) diseases associated with quantitative and/or qualitative changes of sleep architecture.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.smrv.2012.01.004 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
A carnitine transporter at the blood-brain barrier modulates sleep via glial lipid metabolism in .
Proc Natl Acad Sci U S A
January 2025
Department of Cell Biology, Emory University, Atlanta, GA 30322.
To regulate brain function, peripheral compounds must traverse the blood-brain barrier (BBB), an interface between the brain and the circulatory system. To determine whether specific transport mechanisms are relevant for sleep, we conducted a BBB-specific inducible RNAi knockdown (iKD) screen for genes affecting sleep in . We observed reduced sleep with knockdown of solute carrier , a carnitine transporter, as determined by isotope flux.
View Article and Find Full Text PDFCalcineurin governs baseline and homeostatic regulations of non-rapid eye movement sleep in mice.
Proc Natl Acad Sci U S A
January 2025
National Institute of Biological Sciences, Beijing 102206, China.
Sleep need accumulates during waking and dissipates during sleep to maintain sleep homeostasis (process S). Besides the regulation of daily (baseline) sleep amount, homeostatic sleep regulation commonly refers to the universal phenomenon that sleep deprivation (SD) causes an increase of sleep need, hence, the amount and intensity of subsequent recovery sleep. The central regulators and signaling pathways that govern the baseline and homeostatic sleep regulations in mammals remain unclear.
View Article and Find Full Text PDFExploring the Effects of Sleep Deprivation on Physical Performance: An EEG Study in the Context of High-Intensity Endurance.
Sports Med Open
January 2025
Department of Physical Education, Tongji University, Shanghai, 200000, China.
Background: While the effects of sleep deprivation on cognitive function are well-documented, its impact on high-intensity endurance performance and underlying neural mechanisms remains underexplored, especially in the context of search and rescue operations where both physical and mental performance are essential. This study examines the neurophysiological basis of sleep deprivation on high-intensity endurance using electroencephalography (EEG). In this crossover study, twenty firefighters were subjected to both sleep deprivation (SD) and normal sleep conditions, with each participant performing endurance treadmill exercise the following morning after each condition.
View Article and Find Full Text PDFAntibiotics for Paediatric Community-Acquired Pneumonia: What is the Optimal Course Duration?
Paediatr Drugs
January 2025
Child and Maternal Health Division, Menzies School of Health Research, Charles Darwin University, Darwin, NT, Australia.
Despite significant global reductions in cases of pneumonia during the last 3 decades, pneumonia remains the leading cause of post-neonatal mortality in children aged <5 years. Beyond the immediate disease burden it imposes, pneumonia contributes to long-term morbidity, including lung function deficits and bronchiectasis. Viruses are the most common cause of childhood pneumonia, but bacteria also play a crucial role.
View Article and Find Full Text PDFPatient-centered outcomes for clinical trials in chronic rhinosinusitis with or without nasal polyps and allergic fungal rhinosinusitis.
J Patient Rep Outcomes
January 2025
Sanofi US Services, Inc., Bridgewater, NJ, USA.
Background: Chronic rhinosinusitis (inclusive of subtypes with nasal polyps [CRSwNP], without nasal polyps [CRSsNP], and allergic fungal rhinosinusitis [AFRS]) causes inflammation of the nose mucosa and paranasal sinuses. Unfortunately, evidence supporting use of clinical outcome assessments (COAs) in regulated clinical trials to assess key measurement concepts of these conditions is limited.
Objective: To identify key disease-related symptoms and impacts, potential outcomes of interest for new treatments, and COAs available to measure those outcomes among adult and adolescent individuals living with CRSwNP, CRSsNP, and AFRS.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!