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Susan Redline - One of the best experts on this subject based on the ideXlab platform.
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Slow Wave Sleep and mri markers of brain aging in a community based sample
Neurology, 2021Co-Authors: A Baril, Susan Redline, Alexa S Beiser, Vincent Mysliwiec, Erlan Sanchez, Charles Decarli, Daniel J Gottlieb, Pauline Maillard, Jose R Romero, Claudia L SatizabalAbstract:Objective To test the hypothesis that reduced Slow-Wave Sleep, or N3 Sleep, which is thought to underlie the restorative functions of Sleep, is associated with MRI markers of brain aging, we evaluated this relationship in the community-based Framingham Heart Study Offspring cohort using polysomnography and brain MRI. Methods We studied 492 participants (age 58.8 ± 8.8 years, 49.4% male) free of neurological diseases who completed a brain MRI scan and in-home overnight polysomnography to assess Slow-Wave Sleep (absolute duration and percentage of total Sleep). Volumes of total brain, total cortical, frontal cortical, subcortical gray matter, hippocampus, and white matter hyperintensities were investigated as a percentage of intracranial volume, and the presence of covert brain infarcts was evaluated. Linear and logistic regression models were adjusted for age, age squared, sex, time interval between polysomnography and MRI (3.3 ± 1.0 years), APOE e4 carrier status, stroke risk factors, Sleeping pill use, body mass index, and depression. Results Less Slow-Wave Sleep was associated with lower cortical brain volume (absolute duration, β [standard error] = 0.20 [0.08], p = 0.015; percentage, 0.16 [0.08], p = 0.044), lower subcortical brain volume (percentage, 0.03 [0.02], p = 0.034), and higher white matter hyperintensities volume (absolute duration, −0.12 [0.05], p = 0.010; percentage, −0.10 [0.04], p = 0.033). Slow-Wave Sleep duration was not associated with hippocampal volume or the presence of covert brain infarcts. Conclusion Loss of Slow-Wave Sleep might facilitate accelerated brain aging, as evidence by its association with MRI markers suggestive of brain atrophy and injury. Alternatively, subtle injuries and accelerated aging might reduce the ability of the brain to produce Slow-Wave Sleep.
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Slow Wave Sleep and mri markers of brain aging in a community based sample
Neurology, 2021Co-Authors: A Baril, Susan Redline, Alexa S Beiser, Vincent Mysliwiec, Erlan Sanchez, Charles Decarli, Daniel J Gottlieb, Pauline Maillard, Jose R Romero, Claudia L SatizabalAbstract:Objective: To test the hypothesis that reduced Slow-Wave Sleep, or N3 Sleep, which is thought to underlie the restorative functions of Sleep, is associated with MRI markers of brain aging, we evaluated this relationship in the community-based Framingham Heart Study Offspring cohort using polysomnography and brain MRI. Methods: We studied 492 participants (58.8 ± 8.8 years, 49.4% male) free of neurological diseases who completed a brain MRI scan and in-home overnight polysomnography to assess Slow-Wave Sleep (absolute duration and percentage of total Sleep). Volumes of total brain, total cortical, frontal cortical, subcortical gray matter, hippocampus, and white matter hyperintensities were investigated as a percentage of intracranial volume and the presence of covert brain infarcts was evaluated. Linear and logistic regression models were adjusted for age, age squared, sex, time interval between polysomnography and MRI (3.3 ± 1.0 years), APOE4 carrier status, stroke risk factors, Sleeping pill use, body mass index and depression. Results: Less Slow-Wave Sleep was associated with lower cortical brain volume (absolute duration, β[standard error]: 0.20[0.08], p=0.015; percentage, 0.16[0.08], p=0.044), lower subcortical brain volume (percentage, 0.03[0.02], p=0.034), and higher white matter hyperintensities volume (absolute duration, -0.12[0.05], p=0.010; percentage -0.10[0.04], p=0.033). Slow-Wave Sleep duration was not associated with hippocampal volume or the presence of covert brain infarcts. Conclusion: Loss of Slow-Wave Sleep might facilitate accelerated brain aging, as evidence by its association with MRI markers suggestive of brain atrophy and injury. Alternatively, subtle injuries and accelerated aging might reduce the ability of the brain to produce Slow-Wave Sleep.
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Sleep, Slow-Wave Sleep, and Blood Pressure
Current hypertension reports, 2012Co-Authors: Sogol Javaheri, Susan RedlineAbstract:There is increasing evidence that alterations in Sleep continuity due to central nervous system arousal and/or reductions in deeper stages of Sleep adversely affect blood pressure and contribute to hypertension. Disturbed Sleep also blunts the normal nocturnal dip in blood pressure and may lead to sustained daytime hypertension as well. Nocturnal drops in blood pressure result from increased parasympathetic and reduced sympathetic activity during Sleep. Slow-Wave Sleep, considered to be the most “restorative,” is the specific Sleep state associated with the largest decline in sympathetic activity. The time in Slow-Wave Sleep declines with age as well as in association with other health problems. A reduction in the time in Slow-Wave Sleep has recently been reported to predict increased incident hypertension. The mechanisms by which this occurs have not been well described but may include alterations in dipping patterns, sympathetic nervous system activity, corticotrophin pathways, and the renin–angiotensin system. This article reviews the overall association between Sleep and hypertension, with a specific focus on Slow-Wave Sleep, a possible novel target for future blood pressure interventions.
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decreased Slow Wave Sleep increases risk of developing hypertension in elderly men
Hypertension, 2011Co-Authors: Maple M Fung, Sonia Ancoliisrael, Susan Redline, Katherine W Peters, Michael G Ziegler, Elizabeth Barrettconnor, Katie L StoneAbstract:The importance of Sleep to health and cardiovascular disease has become increasingly apparent. Sleep disordered breathing (SDB), Sleep duration, and Sleep architecture may all influence metabolism and neurohormonal systems, yet no prior study has evaluated these Sleep characteristics concurrently in relation to incident hypertension. Our objective was to determine if incident hypertension is associated with polysomnography (PSG) measures of SDB, Sleep duration, and Sleep architecture in older men. Participants were784 community dwelling, ambulatory men ≥65 years (mean age 75.1±4.9 years) from the Outcomes of Sleep Disorders in Older Men Study (MrOs Sleep Study) who did not have hypertension at the time of their in-home PSG Sleep studies (2003-2005); and who returned for follow-up (2007-2009). Of 784 older men included in this report, 243 met criteria for incident hypertension after a mean follow-up of 3.4 years. In unadjusted analyses, incident hypertension was associated with increased hypoxemia, increased Sleep stages N1 and N2 and decreased stage N3 (Slow Wave Sleep, SWS). After adjustment for age, non-white race, study site, and body mass index, the only Sleep index to remain significantly associated with incident HTN was SWS percent (odds ratio for lowest to highest quartile of SWS: 1.83, 95% CI 1.18, 2.85). No attenuation of this association was seen after accounting for Sleep duration, Sleep fragmentation and indices of SDB. Percentage time in SWS was inversely associated with incident HTN, independent of Sleep duration and fragmentation, and SDB. Selective deprivation of SWS may contribute to adverse blood pressure in older men.
Reto Huber - One of the best experts on this subject based on the ideXlab platform.
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remission of encephalopathy with status epilepticus eses during Sleep renormalizes regulation of Slow Wave Sleep
Epilepsia, 2017Co-Authors: Bigna K Bolsterli, Reto Huber, Elena Gardella, Elena Pavlidis, Flavia M Wehrle, C A Tassinari, Guido RubboliAbstract:OBJECTIVE: In previous studies, we showed an altered overnight decrease of non-rapid-eye-movement (NREM) Sleep Slow Waves in children with encephalopathy related to status epilepticus during Sleep (ESES). Here, we test the hypothesis that these alterations renormalize after remission of ESES. Because overnight decrease of Slow Waves has been linked to brain recovery and cognition, we investigate whether cognitive outcome is related to overnight changes of Slow Waves. METHODS: We performed a retrospective analysis of longitudinal overnight electroencephalography (EEG) in 10 patients with idiopathic ESES. Automated Slow Wave detection and calculation of slope of Slow Waves during the first and last hour of NREM Sleep were employed. Intraindividual comparisons were undertaken of the slope during active phase and after remission of ESES, and between patients after remission of ESES and healthy controls. Explorative analysis of the relationship between Slow Wave slope and cognitive outcome was performed. RESULTS: The slope of Slow Waves did not decrease significantly across the night during active ESES, particularly at the spike focus. After remission of ESES, the slope decreased significantly overnight. Compared to controls, there was no difference in overnight slope decrease. Association between slope and neuropsychological outcome showed best cognitive outcome after remission in those children (n = 3) who showed some degree of slope decline during active ESES. SIGNIFICANCE: This study provides evidence that alterations of overnight changes of NREM-Sleep Slow Waves during active ESES are reversible when ESES resolves, and that the severity of neuropsychological compromise might be related to the extent of Slow Wave impairment during ESES. Our findings suggest that analysis of Slow Waves might serve as a prognostic factor regarding cognitive outcome. ESES may serve as disease model of pathologic Slow Wave Sleep and our results might be expanded to epilepsies with spike Wave activation in Slow Wave Sleep not only in children but also in adults.
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impaired Slow Wave Sleep downscaling in encephalopathy with status epilepticus during Sleep eses
Clinical Neurophysiology, 2011Co-Authors: Bigna K Bolsterli, Bernhard Schmitt, T Bast, Hanne Critelli, Jakob Heinzle, Oskar G Jenni, Reto HuberAbstract:Abstract Objective “Encephalopathy related to electrical status epilepticus during Slow Wave Sleep” (ESES) is characterised by the electroencephalographic pattern of continuous spike Waves during Slow Wave Sleep (CSWS) and variable neuropsychological impairments. The synaptic homeostasis hypothesis predicts that the strength of synapses is decreased during Sleep. The slope of Slow Waves during NREM Sleep best reflects this “downscaling”. Methods In a retrospective case control study, we analysed the time course of the slope of EEG Slow Waves of nine patients with ESES. The patients showed continuous spike Waves (>85%) associated with regression or stagnation of cognitive functions. The data of the patient group were compared to nine healthy age and gender matched controls. Results In control subjects we found the expected decrease of the slope of Slow Waves from the first to the last hour of Sleep (17.2% decrease, p Conclusions This finding may reflect a disruption of the downscaling process during Sleep, which may contribute to the developmental regression in these children. Significance Thus, our findings contribute to the understanding of the pathomechanisms leading to the regression observed in children with ESES and support the view that the goal of the treatment in children with ESES should not only be to reduce seizures, but also to resolve the continuous spike Wave activity.
Sonia Ancoliisrael - One of the best experts on this subject based on the ideXlab platform.
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decreased Slow Wave Sleep increases risk of developing hypertension in elderly men
Hypertension, 2011Co-Authors: Maple M Fung, Sonia Ancoliisrael, Susan Redline, Katherine W Peters, Michael G Ziegler, Elizabeth Barrettconnor, Katie L StoneAbstract:The importance of Sleep to health and cardiovascular disease has become increasingly apparent. Sleep disordered breathing (SDB), Sleep duration, and Sleep architecture may all influence metabolism and neurohormonal systems, yet no prior study has evaluated these Sleep characteristics concurrently in relation to incident hypertension. Our objective was to determine if incident hypertension is associated with polysomnography (PSG) measures of SDB, Sleep duration, and Sleep architecture in older men. Participants were784 community dwelling, ambulatory men ≥65 years (mean age 75.1±4.9 years) from the Outcomes of Sleep Disorders in Older Men Study (MrOs Sleep Study) who did not have hypertension at the time of their in-home PSG Sleep studies (2003-2005); and who returned for follow-up (2007-2009). Of 784 older men included in this report, 243 met criteria for incident hypertension after a mean follow-up of 3.4 years. In unadjusted analyses, incident hypertension was associated with increased hypoxemia, increased Sleep stages N1 and N2 and decreased stage N3 (Slow Wave Sleep, SWS). After adjustment for age, non-white race, study site, and body mass index, the only Sleep index to remain significantly associated with incident HTN was SWS percent (odds ratio for lowest to highest quartile of SWS: 1.83, 95% CI 1.18, 2.85). No attenuation of this association was seen after accounting for Sleep duration, Sleep fragmentation and indices of SDB. Percentage time in SWS was inversely associated with incident HTN, independent of Sleep duration and fragmentation, and SDB. Selective deprivation of SWS may contribute to adverse blood pressure in older men.
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pimavanserin tartrate a 5 ht2a receptor inverse agonist increases Slow Wave Sleep as measured by polysomnography in healthy adult volunteers
Sleep Medicine, 2011Co-Authors: Sonia Ancoliisrael, Kimberly E Vanover, David M. Weiner, Robert E. Davis, Daniel P. KammenAbstract:Abstract Objective Determine the effects of pimavanserin tartrate [ACP-103; N -(4-flurophenylmethyl)- N -(1-methylpiperidin-4-yl)- N ′-(4-(2-methylpropyloxy)phenylmethyl)carbamide], a selective serotonin 5-HT 2A receptor inverse agonist, on Slow Wave Sleep (SWS), other Sleep parameters, and attention/vigilance. Methods Forty-five healthy adults were randomized to pimavanserin (1, 2.5, 5, or 20mg) or placebo in a double-blind fashion ( n =9/group). Pimavanserin or placebo was administered once daily in the morning for 13 consecutive days. The effects of pimavanserin were measured after the first dose and again after 13days. Sleep parameters were measured by polysomnography. Effects on attention/vigilance were measured by a continuous performance task. Results Compared to placebo, pimavanserin significantly increased SWS following single and multiple dose administration. Pimavanserin also decreased number of awakenings. PSG variables not affected by pimavanserin included Sleep period time, total Sleep time, Sleep onset latency, number of stage shifts, total time awake, early morning wake, and microarousal index. Changes in Sleep architecture parameters, Sleep profile parameters, and spectral power density parameters were consistent with a selective increase in SWS. Pimavanserin did not adversely affect performance on the continuous performance test measured in the evening before or morning after polysomnography. Conclusions These data suggest that pimavanserin selectively increases Slow Wave Sleep and decreases awakenings, an effect that does not diminish with repeated administration.
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pimavanserin tartrate a 5 ht2a receptor inverse agonist increases Slow Wave Sleep as measured by polysomnography in healthy adult volunteers
Sleep Medicine, 2011Co-Authors: Sonia Ancoliisrael, Kimberly E Vanover, David M. Weiner, Robert E. Davis, Daniel P. KammenAbstract:Abstract Objective Determine the effects of pimavanserin tartrate [ACP-103; N -(4-flurophenylmethyl)- N -(1-methylpiperidin-4-yl)- N ′-(4-(2-methylpropyloxy)phenylmethyl)carbamide], a selective serotonin 5-HT 2A receptor inverse agonist, on Slow Wave Sleep (SWS), other Sleep parameters, and attention/vigilance. Methods Forty-five healthy adults were randomized to pimavanserin (1, 2.5, 5, or 20mg) or placebo in a double-blind fashion ( n =9/group). Pimavanserin or placebo was administered once daily in the morning for 13 consecutive days. The effects of pimavanserin were measured after the first dose and again after 13days. Sleep parameters were measured by polysomnography. Effects on attention/vigilance were measured by a continuous performance task. Results Compared to placebo, pimavanserin significantly increased SWS following single and multiple dose administration. Pimavanserin also decreased number of awakenings. PSG variables not affected by pimavanserin included Sleep period time, total Sleep time, Sleep onset latency, number of stage shifts, total time awake, early morning wake, and microarousal index. Changes in Sleep architecture parameters, Sleep profile parameters, and spectral power density parameters were consistent with a selective increase in SWS. Pimavanserin did not adversely affect performance on the continuous performance test measured in the evening before or morning after polysomnography. Conclusions These data suggest that pimavanserin selectively increases Slow Wave Sleep and decreases awakenings, an effect that does not diminish with repeated administration.
Daniel P. Kammen - One of the best experts on this subject based on the ideXlab platform.
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pimavanserin tartrate a 5 ht2a receptor inverse agonist increases Slow Wave Sleep as measured by polysomnography in healthy adult volunteers
Sleep Medicine, 2011Co-Authors: Sonia Ancoliisrael, Kimberly E Vanover, David M. Weiner, Robert E. Davis, Daniel P. KammenAbstract:Abstract Objective Determine the effects of pimavanserin tartrate [ACP-103; N -(4-flurophenylmethyl)- N -(1-methylpiperidin-4-yl)- N ′-(4-(2-methylpropyloxy)phenylmethyl)carbamide], a selective serotonin 5-HT 2A receptor inverse agonist, on Slow Wave Sleep (SWS), other Sleep parameters, and attention/vigilance. Methods Forty-five healthy adults were randomized to pimavanserin (1, 2.5, 5, or 20mg) or placebo in a double-blind fashion ( n =9/group). Pimavanserin or placebo was administered once daily in the morning for 13 consecutive days. The effects of pimavanserin were measured after the first dose and again after 13days. Sleep parameters were measured by polysomnography. Effects on attention/vigilance were measured by a continuous performance task. Results Compared to placebo, pimavanserin significantly increased SWS following single and multiple dose administration. Pimavanserin also decreased number of awakenings. PSG variables not affected by pimavanserin included Sleep period time, total Sleep time, Sleep onset latency, number of stage shifts, total time awake, early morning wake, and microarousal index. Changes in Sleep architecture parameters, Sleep profile parameters, and spectral power density parameters were consistent with a selective increase in SWS. Pimavanserin did not adversely affect performance on the continuous performance test measured in the evening before or morning after polysomnography. Conclusions These data suggest that pimavanserin selectively increases Slow Wave Sleep and decreases awakenings, an effect that does not diminish with repeated administration.
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pimavanserin tartrate a 5 ht2a receptor inverse agonist increases Slow Wave Sleep as measured by polysomnography in healthy adult volunteers
Sleep Medicine, 2011Co-Authors: Sonia Ancoliisrael, Kimberly E Vanover, David M. Weiner, Robert E. Davis, Daniel P. KammenAbstract:Abstract Objective Determine the effects of pimavanserin tartrate [ACP-103; N -(4-flurophenylmethyl)- N -(1-methylpiperidin-4-yl)- N ′-(4-(2-methylpropyloxy)phenylmethyl)carbamide], a selective serotonin 5-HT 2A receptor inverse agonist, on Slow Wave Sleep (SWS), other Sleep parameters, and attention/vigilance. Methods Forty-five healthy adults were randomized to pimavanserin (1, 2.5, 5, or 20mg) or placebo in a double-blind fashion ( n =9/group). Pimavanserin or placebo was administered once daily in the morning for 13 consecutive days. The effects of pimavanserin were measured after the first dose and again after 13days. Sleep parameters were measured by polysomnography. Effects on attention/vigilance were measured by a continuous performance task. Results Compared to placebo, pimavanserin significantly increased SWS following single and multiple dose administration. Pimavanserin also decreased number of awakenings. PSG variables not affected by pimavanserin included Sleep period time, total Sleep time, Sleep onset latency, number of stage shifts, total time awake, early morning wake, and microarousal index. Changes in Sleep architecture parameters, Sleep profile parameters, and spectral power density parameters were consistent with a selective increase in SWS. Pimavanserin did not adversely affect performance on the continuous performance test measured in the evening before or morning after polysomnography. Conclusions These data suggest that pimavanserin selectively increases Slow Wave Sleep and decreases awakenings, an effect that does not diminish with repeated administration.
Penelope A Lewis - One of the best experts on this subject based on the ideXlab platform.
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complementary roles of Slow Wave Sleep and rapid eye movement Sleep in emotional memory consolidation
Cerebral Cortex, 2015Co-Authors: Scott A Cairney, Simon J Durrant, Rebecca Power, Penelope A LewisAbstract:Although rapid eye movement Sleep (REM) is regularly implicated in emotional memory consolidation, the role of Slow-Wave Sleep (SWS) in this process is largely uncharacterized. In the present study, we investigated the relative impacts of nocturnal SWS and REM upon the consolidation of emotional memories using functional magnetic resonance imaging (fMRI) and polysomnography (PSG). Participants encoded emotionally positive, negative, and neutral images (remote memories) before a night of PSG-monitored Sleep. Twenty-four hours later, they encoded a second set of images (recent memories) immediately before a recognition test in an MRI scanner. SWS predicted superior memory for remote negative images and a reduction in right hippocampal responses during the recollection of these items. REM, however, predicted an overnight increase in hippocampal–neocortical connectivity associated with negative remote memory. These findings provide physiological support for sequential views of Sleep-dependent memory processing, demonstrating that SWS and REM serve distinct but complementary functions in consolidation. Furthermore, these findings extend those ideas to emotional memory by showing that, once selectively reorganized away from the hippocampus during SWS, emotionally aversive representations undergo a comparably targeted process during subsequent REM.
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cued memory reactivation during Slow Wave Sleep promotes explicit knowledge of a motor sequence
The Journal of Neuroscience, 2014Co-Authors: James N Cousins, Wael Elderedy, Laura M Parkes, Nora Hennies, Penelope A LewisAbstract:Memories are gradually consolidated after initial encoding, and this can sometimes lead to a transition from implicit to explicit knowledge. The exact physiological processes underlying this reorganization remain unclear. Here, we used a serial reaction time task to determine whether targeted memory reactivation (TMR) of specific memory traces during Slow-Wave Sleep promotes the emergence of explicit knowledge. Human participants learned two 12-item sequences of button presses (A and B). These differed in both cue order and in the auditory tones associated with each of the four fingers (one sequence had four higher-pitched tones). Subsequent overnight Sleep was monitored, and the tones associated with one learned sequence were replayed during Slow-Wave Sleep. After waking, participants demonstrated greater explicit knowledge (p = 0.005) and more improved procedural skill (p = 0.04) for the cued sequence relative to the uncued sequence. Furthermore, fast spindles (13.5–15 Hz) at task-related motor regions predicted overnight enhancement in procedural skill (r = 0.71, p = 0.01). Auditory cues had no effect on post-Sleep memory performance in a control group who received TMR before Sleep. These findings suggest that TMR during Sleep can alter memory representations and promote the emergence of explicit knowledge, supporting the notion that reactivation during Sleep is a key mechanism in this process.
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targeted memory reactivation during Slow Wave Sleep facilitates emotional memory consolidation
Sleep, 2014Co-Authors: Scott A Cairney, Simon J Durrant, Johan Hulleman, Penelope A LewisAbstract:Study Objectives: To investigate the mechanisms by which auditory targeted memory reactivation (TMR) during Slow Wave Sleep (SWS) influences the consolidation of emotionally negative and neutral memories. Design: Each of 72 (36 negative, 36 neutral) picture-location associations were encoded with a semantically related sound. During a subsequent nap, half of the sounds were replayed in SWS, before picture-location recall was examined in a final test. Setting: Manchester Sleep Laboratory, University of Manchester. Participants: 15 adults (3 male) mean age = 20.40 (standard deviation ± 3.07). Interventions: TMR with auditory cues during SWS. Measurements and Results: Performance was assessed by memory accuracy and recall response times (RTs). Data were analyzed with a 2 (sound: replayed/not replayed) × 2 (emotion: negative/neutral) repeated measures analysis of covariance with SWS duration, and then SWS spindles, as the mean-centered covariate. Both analyses revealed a significant three-way interaction for RTs but not memory accuracy. Critically, SWS duration and SWS spindles predicted faster memory judgments for negative, relative to neutral, picture locations that were cued with TMR. Conclusions: TMR initiates an enhanced consolidation process during subsequent SWS, wherein Sleep spindles mediate the selective enhancement of reactivated emotional memories.
