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Slow oscillations and sleep spindles are hallmarks of the EEG during slow-wave sleep (SWS). Both oscillatory events, especially when co-occurring in the constellation of spindles nesting in the slow oscillation upstate, are considered to support memory formation and underlying synaptic plasticity. The regulatory mechanisms of this function at the circuit level are poorly understood. Here, using two-photon imaging in mice, we relate EEG-recorded slow oscillations and spindles to calcium signals recorded from the soma of cortical putative pyramidal-like (Pyr) cells and neighboring parvalbumin-positive interneurons (PV-Ins) or somatostatin-positive interneurons (SOM-Ins). Pyr calcium activity was increased more than threefold when spindles co-occurred with slow oscillation upstates compared with slow oscillations or spindles occurring in isolation. Independent of whether or not a spindle was nested in the slow oscillation upstate, the slow oscillation downstate was preceded by enhanced calcium signal in SOM-Ins that vanished during the upstate, whereas spindles were associated with strongly increased PV-In calcium activity. Additional wide-field calcium imaging of Pyr cells confirmed the enhanced calcium activity and its widespread topography associated with spindles nested in slow oscillation upstates. In conclusion, when spindles are nested in slow oscillation upstates, maximum Pyr activity appears to concur with strong perisomatic inhibition of Pyr cells via PV-Ins and low dendritic inhibition via SOM-Ins (i.e., conditions that might optimize synaptic plasticity within local cortical circuits).

Sleep is essential for memory formation. Active systems consolidation maintains that memory traces that are initially stored in a transient store such as the hippocampus are gradually redistributed towards more permanent storage sites such as the cortex during sleep replay. The complementary synaptic homeostasis theory posits that weak memory traces are erased during sleep through a competitive down-selection mechanism, ensuring the brain’s capability to learn new information. We discuss evidence from neuropharmacological experiments in humans to show how major neurotransmitters and neuromodulators are implicated in these memory processes. As to the major excitatory neurotransmitter glutamate that plays a prominent role in inducing synaptic consolidation, we show that these processes, while strengthening cortical memory traces during sleep, are insufficient to explain the consolidation of hippocampus-dependent declarative memories. In the inhibitory GABAergic system, we will offer insights how drugs may alter the intricate interplay of sleep oscillations that have been identified to be crucial for strengthening memories during sleep. Regarding the dopaminergic reward system, we will show how it is engaged during sleep replay, but that dopaminergic neuromodulation likely plays a side role for enhancing relevant memories during sleep. Also, we briefly go into basic evidence on acetylcholine and cortisol whose low tone during slow wave sleep (SWS) is crucial in supporting hippocampal-to-neocortical memory transmission. Finally, we will outline how these insights can be used to improve treatment of neuropsychiatric disorders focusing mainly on anxiety disorders, depression, and addiction that are strongly related to memory processing.

There is significant interest in altering the course of cardiometabolic disease development via gut microbiomes. Nevertheless, the highly abundant phage members of the complex gut ecosystem -which impact gut bacteria- remain understudied. Here, we show gut virome changes associated with metabolic syndrome (MetS), a highly prevalent clinical condition preceding cardiometabolic disease, in 196 participants by combined sequencing of bulk whole genome and virus like particle communities. MetS gut viromes exhibit decreased richness and diversity. They are enriched in phages infecting Streptococcaceae and Bacteroidaceae and depleted in those infecting Bifidobacteriaceae . Differential abundance analysis identifies eighteen viral clusters (VCs) as significantly associated with either MetS or healthy viromes. Among these are a MetS-associated Roseburia VC that is related to healthy control-associated Faecalibacterium and Oscillibacter VCs. Further analysis of these VCs revealed the Candidatus Heliusviridae , a highly widespread gut phage lineage found in 90+% of participants. The identification of the temperate Ca. Heliusviridae provides a starting point to studies of phage effects on gut bacteria and the role that this plays in MetS. Here, the authors characterize gut viromes in a cohort of individuals with metabolic syndrome, which they find associated with a highly widespread family of gut bacteriophages they name Candidatus Heliusviridae .

Large differences in cardiovascular disease (CVD) morbidity and mortality exist between migrant populations and host populations. Understanding the drivers behind these disparities may help to mitigate the unequal burden of CVD and identify new causal pathways that contribute to CVD risk in the population at large.

There is a long-standing division in memory research between hippocampus-dependent memory and non-hippocampus-dependent memory, as only the latter can be acquired and retrieved in the absence of normal hippocampal function 1 , 2 . Consolidation of hippocampus-dependent memory, in particular, is strongly supported by sleep 3 – 5 . Here we show that the formation of long-term representations in a rat model of non-hippocampus-dependent memory depends not only on sleep but also on activation of a hippocampus-dependent mechanism during sleep. Rats encoded non-hippocampus-dependent (novel-object recognition 6 – 8 ) and hippocampus-dependent (object–place recognition) memories before a two-hour period of sleep or wakefulness. Memory was tested either immediately thereafter or remotely (after one or three weeks). Whereas object–place recognition memory was stronger for rats that had slept after encoding (rather than being awake) at both immediate and remote testing, novel-object recognition memory profited from sleep only three weeks after encoding, at which point it was preserved in rats that had slept after encoding but not in those that had been awake. Notably, inactivation of the hippocampus during post-encoding sleep by intrahippocampal injection of muscimol abolished the sleep-induced enhancement of remote novel-object recognition memory. By contrast, muscimol injection before remote retrieval or memory encoding had no effect on test performance, confirming that the encoding and retrieval of novel-object recognition memory are hippocampus-independent. Remote novel-object recognition memory was associated with spindle activity during post-encoding slow-wave sleep, consistent with the view that neuronal memory replay during slow-wave sleep contributes to long-term memory formation. Our results indicate that the hippocampus has an important role in long-term consolidation during sleep even for memories that have previously been considered hippocampus-independent. Hippocampal activity during a period of sleep after memory encoding is crucial for forming long-term memories in rats, even for types of memory considered not to be hippocampus-dependent.

In 2008, Vyazovskiy et al. published a seminal study demonstrating that sleep induces a widespread downscaling of synapses that counters the synaptic upscaling that occurred during prior wakefulness. The study laid the groundwork for current research into the ‘where’ and ‘when’ of homeostatic neuronal network regulation during sleep.

Abstract Background Non-communicable diseases (NCDs) remain a major challenge in the 21st century. High-income countries (HICs) populations are ethnically and culturally diverse due to international migration. Evidence suggests that NCDs rates differ between migrants and the host populations in HICs. This paper presents a review of NCDs burden among migrant groups in HICs in Europe, North America and Australia with a major focus on cardiovascular diseases (CVDs), cancer and diabetes. Methods We performed a narrative review consisting of scholarly papers published between 1960 until 2018. Results CVD risk differs by country of origin, country of destination and duration of residence. For example, stroke is more common in sub-Sahara African and South-Asian migrants, but lower in North African and Chinese migrants. Chinese migrants, however, have a higher risk of haemorrhagic stroke despite the lower rate of overall stroke. Coronary heart disease (CHD) is more common in South-Asian migrants, but less common in sub-Saharan and north African migrants although the lower risk of CHD in these population is waning. Diabetes risk is higher in all migrants and migrants seem to develop diabetes at an earlier age than the host populations. Migrants in general have lower rates of overall cancer morbidity and mortality than the host populations in Europe. However, migrants have a higher infectious disease-related cancers than the host populations in Europe. In North America, the picture is more complex. Data from cross-national comparisons indicate that migration-related lifestyle changes associated with the lifestyle of the host population in the country of settlement may influence NCDs risk among migrants in a very significant way. Conclusion With exception of diabetes, which is consistently higher in all migrant groups than in the host populations, the burden of NCDs among migrants seems to depend on the migrant group, country of settlement and NCD type. This suggests that more work is needed to disentangle the key migration-related lifestyle changes and contextual factors that may be driving the differential risk of NCDs among migrants in order to assist prevention and clinical management of NCDs in these populations.

Sleep is essential for health. Slow wave sleep (SWS), the deepest sleep stage hallmarked by electroencephalographic slow oscillations (SOs), appears of particular relevance here. SWS is associated with a unique endocrine milieu comprising minimum cortisol and high aldosterone, growth hormone (GH), and prolactin levels, thereby presumably fostering efficient adaptive immune responses. Yet, whether SWS causes these changes is unclear. Here we enhance SOs in men by auditory closed-loop stimulation, i.e., by delivering tones in synchrony with endogenous SOs. Stimulation intensifies the hormonal milieu characterizing SWS (mainly by further reducing cortisol and increasing aldosterone levels) and reduces T and B cell counts, likely reflecting a redistribution of these cells to lymphoid tissues. GH remains unchanged. In conclusion, closed-loop stimulation of SOs is an easy-to-use tool for probing SWS functions, and might also bear the potential to ameliorate conditions like depression and aging, where disturbed sleep coalesces with specific hormonal and immunological dysregulations. Circulating hormones undergo fluctuations during sleep. Here, the authors increase electroencephalographic slow oscillations (SO) during sleep in men using an auditory closed-loop stimulation, and show that the circulating level of cortisol, aldosterone and immune cell count can be altered.

Viruses are core components of the human microbiome, impacting health through interactions with gut bacteria and the immune system. Most human microbiome viruses are bacteriophages, which exclusively infect bacteria. Until recently, most gut virome studies focused on low taxonomic resolution (e.g., viral operational taxonomic units), hampering population-level analyses. We previously identified an expansive and widespread bacteriophage lineage in inhabitants of Amsterdam, the Netherlands. Here, we study their biodiversity and evolution in various human populations. Based on a phylogeny using sequences from six viral genome databases, we propose the Candidatus order Heliusvirales . We identify heliusviruses in 82% of 5441 individuals across 39 studies, and in nine metagenomes from humans that lived in Europe and North America between 1000 and 5000 years ago. We show that a large lineage started to diversify when Homo sapiens first appeared some 300,000 years ago. Ancient peoples and modern hunter-gatherers have distinct Ca. Heliusvirales populations with lower richness than modern urbanized people. Urbanized people suffering from type 1 and type 2 diabetes, as well as inflammatory bowel disease, have higher Ca. Heliusvirales richness than healthy controls. We thus conclude that these ancient core members of the human gut virome have thrived with increasingly westernized lifestyles. Here, based on phylogeny analyses using sequences from six viral genome databases, the authors study the biodiversity and evolution of a new bacteriophage lineage, Candidatus order Heliusvirales , and identify heliusviruses in 82% of 5,441 individuals across 39 studies, and in nine metagenomes from humans that lived in Europe and North America between 1,000 and 5,000 years ago, revealing associations with human diseases.

The retrieval of spatial memory is behaviorally often assessed in tasks like the classical Object-Place-Recognition (OPR) task that requires an updating of memory. The neural dynamics across interconnected brain regions underlying retrieval processing in such tasks, are not well understood. Here, we examined in rats the neural correlates of retrieval processing in the OPR task by comparing a condition of successful OPR retrieval, in which the displaced object during the retrieval phase (3-hours after encoding) induced a spatial memory updating (OPR condition), with a stationary (STA) control condition in which the object configuration at retrieval was identical to encoding and, therefore, did not require spatial updating. Importantly, both conditions involved re-exposure to the previously encountered objects and context, but only the OPR condition imposed demands on updating the stored spatial representation. Expression of c-Fos (as an activity marker) and GAD67 (to identify inhibitory interneurons) was assessed at retrieval in hippocampal subfields, mPFC areas, thalamic nuclei, and posterior cortical regions. Rats in the OPR condition exhibited robust object-place discrimination and enhanced rearing behavior compared to the STA condition. Regional c-Fos activation levels were largely comparable between OPR and STA conditions across hippocampal, cortical, and thalamic regions. However, the OPR condition showed a region-specific increase in the proportion of GAD67-positive active neurons in proximal CA1. Together, these findings identify a specific pattern of inhibitory engagement implicating selective hippocampal inhibitory recruitment in supporting retrieval-driven spatial memory updating rather than elevated global activation.