Biology subjects

Weber, F. D.

Publications and source records attributed to Weber, F. D..

5 recordsLinked to original sources

bioRxiv2026

Natural sleep, but not propofol-induced anesthesia preserves spatial and procedural memory consolidation

Propofol-induced general anesthesia and natural sleep are both associated with GABA-A-ergic inhibition and slow-wave activity. Whereas sleep actively supports memory consolidation, consolidation may be disrupted during anesthesia. Here, we compared EEG and memory data from 19 participants undergoing surgery under propofol-induced anesthesia with data from 17 participants taking a nap. In both groups, participants completed a hippocampus-dependent spatial memory task (Virtual Water Maze) and a procedural memory task (Mirror Tracing) before (pre) and after (post) an interval filled with either anesthesia or sleep. Performance declined from pre to post in the propofol group for both tasks, whereas it remained stable in the sleep group. Slow oscillations (SO) occurred during both non-REM sleep and propofol-induced anesthesia. However, only during non-REM sleep did SOs show increased spindle activity during the SO upstate. Together, these findings suggest that propofol anesthesia disrupts memory consolidation, most likely because SOs under anesthesia lack the spindle coupling that mediates the hippocampal-neocortical information transfer underlying systems memory consolidation.

neuroscience↗

bioRxiv2026

Hippocampal CA1 neurons are crucial for sleep-associated memory formation in humans: The role of theta power during NREM sleep

The formation of long-term memory during sleep depends on the reactivation and redistribution of recently acquired mnemonic information during non-rapid eye movement (NREM) sleep. Animal studies suggest that hippocampal memory replay during slow-wave sleep is coordinated through the interaction of sharp-wave ripples, thalamocortical sleep spindles, and neocortical slow oscillations (SOs). However, direct evidence for the contribution of hippocampal network dynamics to sleep-dependent memory consolidation in humans remains limited. Here, we investigated sleep-dependent memory consolidation in patients (n=13) with transient global amnesia (TGA), a clinical syndrome associated with focal and transient lesions of the hippocampal CA1 region. Patients completed a verbal paired-associative learning task followed by nocturnal polysomnography and subsequent memory retrieval during the acute phase of TGA (acute condition) and again after clinical recovery (follow-up condition). Overnight memory consolidation was significantly impaired during the acute phase compared with the follow-up session. NREM EEG theta power (4-8 Hz) was reduced during the acute phase of TGA. Importantly, increases in theta power from the acute to the follow-up session predicted corresponding improvements in memory consolidation within individuals. In contrast, established NREM markers of sleep-dependent memory consolidation, including sleep spindle density, SO density, and SO-spindle coupling, did not differ between the acute and follow-up conditions. These findings suggest that transient hippocampal CA1 dysfunction disrupts sleep-related hippocampal network dynamics reflected in reduced NREM theta activity, which in turn is associated with impaired memory consolidation. Sleep-related theta oscillations may therefore represent a functional marker of hippocampal network integrity during sleep-dependent memory consolidation in humans.

neuroscience↗

bioRxiv2023

Sustained polyphasic sleep restriction abolishes human growth hormone release

Voluntary sleep restriction is a common phenomenon in industrialized societies aiming to increase time spent awake and thus productivity. We explored how restricting sleep to a radically polyphasic schedule affects neural, cognitive, and endocrine characteristics. Ten young healthy participants were restricted to one 30-min nap opportunity at the end of every 4 hours (i.e., 6 sleep episodes per 24 hours) without any extended core sleep window, which resulted in a cumulative sleep amount of just 2 hours per day (i.e., [~]20 min per bout). All but one participant terminated this schedule during the first three weeks. The remaining participant (a 25-year-old male) succeeded to adhere to a polyphasic schedule for 5 weeks with no apparent impairments in cognitive and psychiatric measures except for psychomotor vigilance. While in-blood cortisol or melatonin release pattern and amounts were unaltered by the polyphasic as compared to monophasic sleep, growth hormone seemed almost entirely abolished (>95% decrease), with the residual release showing a considerably changed polyphasic secretional pattern. While coarse sleep structure appeared intact during polyphasic sleep, REM sleep showed decreased oscillatory and increased aperiodic EEG activity compared to monophasic sleep. Considering the decreased vigilance, abolished growth hormone release, and neurophysiological changes observed, it is doubtful that radically polyphasic sleep schedules can subserve the different functions of sleep to a sufficient degree.

neuroscience↗

bioRxiv2023

Divergent associations of slow-wave sleep vs. REM sleep with plasma amyloid-beta

BackgroundRecent evidence shows that during slow-wave sleep (SWS), the brain is cleared from potentially toxic metabolites, such as the amyloid-beta protein. Poor sleep or elevated cortisol levels can worsen amyloid-beta clearance, potentially leading to the formation of amyloid plaques, a neuropathological hallmark of Alzheimers disease. Here, we explore how nocturnal neural and endocrine activity affects amyloid-beta fluctuations in the peripheral blood as a reflection of cerebral clearance. MethodsSimultaneous polysomnography and all-night blood sampling were acquired in 60 healthy volunteers aged 20-68 years old. Nocturnal plasma concentrations of two amyloid-beta species (amyloid-beta-40 and amyloid-beta-42), cortisol, and growth hormone were assessed every 20 minutes from 23:00-7:00. Amyloid-beta fluctuations were modeled with sleep stages, (non)-oscillatory power, and hormones as predictors while controlling for age and multiple comparisons. Time lags between the predictors and amyloid-beta ranged from 20 to 120min. FindingsThe amyloid-beta-40 and amyloid-beta-42 levels correlated positively with growth hormone concentrations, SWS proportion, slow-wave (0.3-4Hz) oscillatory and high-band (30-48Hz) non-oscillatory power, but negatively with cortisol concentrations and rapid eye movement sleep (REM) proportion measured 40-100min before (all t-values>|3|, p-values<0.003). Older participants showed higher amyloid-beta-40 levels. InterpretationSlow-wave oscillations are associated with higher plasma amyloid-beta levels, reflecting their contribution to cerebral amyloid-beta clearance across the blood-brain barrier. REM sleep is related to decreased amyloid-beta plasma levels; however, this link may reflect passive aftereffects of SWS and not REMs effects per se. Strong associations between cortisol, growth hormone, and amyloid-beta presumably reflect the sleep-regulating role of the corresponding releasing hormones. A positive association between age and amyloid-beta-40 may indicate that peripheral clearance becomes less efficient with age. Our study provides important insights into the specificity of different sleep features effects on brain clearance and suggests that cortisol nocturnal fluctuations may serve as a new marker of clearance efficiency.

neuroscience↗

bioRxiv2021

Non-REM sleep in major depressive disorder

Disturbed sleep is a key symptom in major depressive disorder (MDD). REM sleep alterations are well described in the current fliterature, but little is known about non-REM sleep alterations. Additionally, sleep disturbances relate to a variety of cognitive symptoms in MDD, but which features of non-REM sleep EEG contribute to this, remains unknown. We comprehensively analyzed non-REM sleep EEG features in three independently collected datasets (N=284). These included MDD patients with a broad age range, varying duration and severity of depression, unmedicated or medicated, age- and gender-matched to healthy controls. We explored changes in sleep architecture including sleep stages and cycles, spectral power, sleep spindles, slow waves (SW), and SW-spindle coupling. Next, we analyzed the association of these sleep features with acute measures of depression severity and overnight consolidation of procedural memory. Overall, no major systematic alterations in non-REM sleep architecture were found in patients compared to controls. For the microstructure of non-REM sleep, we observed a higher spindle amplitude in unmedicated patients compared to controls, and after the start of antidepressant medication longer SWs with lower amplitude and a more dispersed SW-spindle coupling. In addition, long-term, but not short-term medication seemed to lower spindle density. Overnight procedural memory consolidation was impaired in medicated patients and associated with lower sleep spindle density. Our results suggest that alterations in non-REM sleep EEG might be more subtle than previously reported. We discuss these findings in the context of antidepressant medication intake and age. Statement of SignificanceDepression affects large and diverse populations worldwide, including their sleep. Most sleep is non-REM sleep, which is vital to cognitive function, including memory. How non-REM is affected during a depression or medical treatment remains poorly investigated. We classified non-REM sleep of depressive patients against healthy controls in unprecedented analysis detail and confidence using the largest dataset published so far while also test sleep alterations associations with impaired memory. Surprisingly, severe depression alone did not alter sleep. We observed severe non-REM sleep alterations only worsening under patient medication, which ultimately coincided with 24-hour memory impairments. Though causal influences of medication on sleep in depressive patients remains to be investigated, this cautions common clinical practice in long-term treatment with antidepressants.

neuroscience↗