Accumulating evidence suggests a central role for sleep spindles in the consolidation of new memories. However, no meta-analysis of the association between sleep spindles and memory performance has been conducted so far. Here, we report meta-analytical evidence for spindle-memory associations and investigate how multiple factors, including memory type, spindle type, spindle characteristics, and EEG topography affect this relationship. The literature search yielded 53 studies reporting 1427 effect sizes, resulting in a small to moderate effect for the average association. We further found that spindle-memory associations were significantly stronger for procedural memory than for declarative memory. Neither spindle types nor EEG scalp topography had an impact on the strength of the spindle-memory relation, but we observed a distinct functional role of global and fast sleep spindles, especially for procedural memory. We also found a moderation effect of spindle characteristics, with power showing the largest effect sizes. Collectively, our findings suggest that sleep spindles are involved in learning, thereby representing a general physiological mechanism for memory consolidation.
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http://dx.doi.org/10.1016/j.neuropsychologia.2023.108661 | DOI Listing |
Ann Clin Transl Neurol
January 2025
Section of Pediatric Neurology and Developmental Neuroscience, Department of Pediatrics, Baylor College of Medicine, Houston, Texas, 77030, USA.
Objective: Rett syndrome (RTT) and MECP2 duplication syndrome (MDS) result from under- and overexpression of MECP2, respectively. Preclinical studies using genetic-based treatment showed robust phenotype recovery for both MDS and RTT. However, there is a risk of converting MDS to RTT, or vice versa, if accurate MeCP2 levels are not achieved.
View Article and Find Full Text PDFSleep Adv
December 2024
Department of Psychiatry, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Study Objectives: Sleep spindles, defining electroencephalographic oscillations of nonrapid eye movement (NREM) stage 2 sleep (N2), mediate sleep-dependent memory consolidation (SDMC). Spindles are also thought to protect sleep continuity by suppressing thalamocortical sensory relay. Schizophrenia is characterized by spindle deficits and a correlated reduction of SDMC.
View Article and Find Full Text PDFNeurology
January 2025
Department of Neurology, Massachusetts General Hospital, Boston.
Background And Objectives: Rolandic epilepsy (RE), the most common childhood focal epilepsy syndrome, is characterized by a transient period of sleep-activated epileptiform activity in the centrotemporal regions and variable cognitive deficits. Sleep spindles are prominent thalamocortical brain oscillations during sleep that have been mechanistically linked to sleep-dependent memory consolidation in animal models and healthy controls. Sleep spindles are decreased in RE and related sleep-activated epileptic encephalopathies.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
Division of Sleep and Circadian Disorders, Brigham and Women's Hospital, Boston, MA 02115.
Sleep spindles are cortical electrical oscillations considered critical for memory consolidation and sleep stability. The timing and pattern of sleep spindles are likely to be important in driving synaptic plasticity during sleep as well as preventing disruption of sleep by sensory and internal stimuli. However, the relative importance of factors such as sleep depth, cortical up/down-state, and temporal clustering in governing sleep spindle dynamics remains poorly understood.
View Article and Find Full Text PDFbioRxiv
December 2024
Department of Neurology, Division of Sleep Medicine, and Program in Neuroscience, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, 02215, USA.
Pain therapies that alleviate both pain and sleep disturbances may be the most effective for pain relief, as both chronic pain and sleep loss render the opioidergic system, targeted by opioids, less sensitive and effective for analgesia. Therefore, we first studied the link between sleep disturbances and the activation of nociceptors in two acute pain models. Activation of nociceptors in both acute inflammatory (AIP) and opto-pain models led to sleep loss, decreased sleep spindle density, and increased sleep fragmentation that lasted 3 to 6 hours.
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