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For decades, it was commonly accepted that the brain is secluded from peripheral immune activity and is self-sufficient for its maintenance and repair. This simplistic perception was based on the presence of resident immune cells, the microglia, and barrier systems within the brain, and the assumption that the central nervous system (CNS) lacks lymphatic drainage. This view was revised with the discoveries that higher functions of the CNS, homeostasis and repair are supported by peripheral innate and adaptive immune cells. The findings of bone marrow-derived immune cells in specialized niches, and the renewed observation that a lymphatic drainage system exists within the brain, further contributed to this revised model. In this Review, we describe the immune niches within the brain, the contribution of professional immune cells to brain functions, the bidirectional relationships between the CNS and the immune system and the relevance of immune components to brain aging and neurodegenerative diseases. Schwartz and colleagues review the immune niches in the brain, the contribution of professional immune cells to brain functions and the relevance of immune components to brain aging and neurodegenerative disease.

The prefrontal cortex (PFC) is implicated in processing of the affective state of others through non-verbal communication. This social cognitive function is thought to rely on an intact cortical neuronal excitatory and inhibitory balance. Here combining in vivo electrophysiology with a behavioral task for affective state discrimination in mice, we show a differential activation of medial PFC (mPFC) neurons during social exploration that depends on the affective state of the conspecific. Optogenetic manipulations revealed a double dissociation between the role of interneurons in social cognition. Specifically, inhibition of mPFC somatostatin (SOM+), but not of parvalbumin (PV+) interneurons, abolishes affective state discrimination. Accordingly, synchronized activation of mPFC SOM+ interneurons selectively induces social discrimination. As visualized by in vivo single-cell microendoscopic Ca2+ imaging, an increased synchronous activity of mPFC SOM+ interneurons, guiding inhibition of pyramidal neurons, is associated with affective state discrimination. Our findings provide new insights into the neurobiological mechanisms of affective state discrimination.

A reduction in hemoglobin levels is common in older subjects. The objective of this study was to investigate the association between changes in blood counts and age in a large outpatient population of adult subjects, in order to verify to what extent such changes may be considered physiological.We examined blood count results in the province of Modena (Italy) from January 2010 to August 2022. Data were analyzed with the platform Anaconda 3, Python 3.7. Appropriate hemoglobin data were extracted from 4,676,003 samples. Hemoglobin levels in subjects over 75 years were largely below lower limits for both sexes (49.3% of 509,834 exams and 35.4% of 704,343 exams for males and females, respectively). The trend was similar in relation to single values per person per year. To exclude patients with some major systemic diseases, we limited our observation to subjects with normal values of serum glucose, creatinine, and alanine transaminase (ALT). In this set of 822,166 analyses, a clinically relevant proportion of older males (nearly 30%) still had hemoglobin values below normal. Such trend was apparent in older age strata. Our findings suggest caution in the interpretation of blood counts in older patients. We therefore advocate a tailored approach in this population.

The Arctic sea-ice-scape is rapidly transforming. Increasing light penetration will initiate earlier seasonal primary production. This earlier growing season may be accompanied by an increase in ice algae and phytoplankton biomass, augmenting the emission of dimethylsulfide and capture of carbon dioxide. Secondary production may also increase on the shelves, although the loss of sea ice exacerbates the demise of sea-ice fauna, endemic fish and megafauna. Sea-ice loss may also deliver more methane to the atmosphere, but warmer ice may release fewer halogens, resulting in fewer ozone depletion events. The net changes in carbon drawdown are still highly uncertain. Despite large uncertainties in these assessments, we expect disruptive changes that warrant intensified long-term observations and modelling efforts.The Arctic is warming and undergoing rapid ice loss. This Perspective considers how changes in sea ice will impact the biogeochemistry and associated ecosystems of the region while calling for more observations to improve our understanding of this complex system.

The Arctic marine ecosystem is shaped by the seasonality of the solar cycle, spanning from 24-h light at the sea surface in summer to 24-h darkness in winter. The amount of light available for under-ice ecosystems is the result of different physical and biological processes that affect its path through atmosphere, snow, sea ice and water. In this article, we review the present state of knowledge of the abiotic (clouds, sea ice, snow, suspended matter) and biotic (sea ice algae and phytoplankton) controls on the underwater light field. We focus on how the available light affects the seasonal cycle of primary production (sympagic and pelagic) and discuss the sensitivity of ecosystems to changes in the light field based on model simulations. Lastly, we discuss predicted future changes in under-ice light as a consequence of climate change and their potential ecological implications, with the aim of providing a guide for future research.

Background For decades, dementia has been characterized by accumulation of waste in the brain and low-grade inflammation. Over the years, emerging studies highlighted the involvement of the immune system in neurodegenerative disease emergence and severity. Numerous studies in animal models of amyloidosis demonstrated the beneficial role of monocyte-derived macrophages in mitigating the disease, though less is known regarding tauopathy. Boosting the immune system in animal models of both amyloidosis and tauopathy, resulted in improved cognitive performance and in a reduction of pathological manifestations. However, a full understanding of the chain of events that is involved, starting from the activation of the immune system, and leading to disease mitigation, remained elusive. Here, we hypothesized that the brain-immune communication pathway that is needed to be activated to combat tauopathy involves monocyte mobilization via the C-C chemokine receptor 2 (CCR2)/CCL2 axis, and additional immune cells, such as CD4 + T cells, including FOXP3 + regulatory CD4 + T cells. Methods We used DM-hTAU transgenic mice, a mouse model of tauopathy, and applied an approach that boosts the immune system, via blocking the inhibitory Programmed cell death protein-1 (PD-1)/PD-L1 pathway, a manipulation previously shown to alleviate disease symptoms and pathology. An anti-CCR2 monoclonal antibody (αCCR2), was used to block the CCR2 axis in a protocol that partially eliminates monocytes from the circulation at the time of anti-PD-L1 antibody (αPD-L1) injection, and for the critical period of their recruitment into the brain following treatment. Results Performance of DM-hTAU mice in short-term and working memory tasks, revealed that the beneficial effect of αPD-L1, assessed 1 month after a single injection, was abrogated following blockade of CCR2. This was accompanied by the loss of the beneficial effect on disease pathology, assessed by measurement of cortical aggregated human tau load using Homogeneous Time Resolved Fluorescence-based immunoassay, and by evaluation of hippocampal neuronal survival. Using both multiparametric flow cytometry, and Cytometry by Time Of Flight, we further demonstrated the accumulation of FOXP3 + regulatory CD4 + T cells in the brain, 12 days following the treatment, which was absent subsequent to CCR2 blockade. In addition, measurement of hippocampal levels of the T-cell chemoattractant, C-X-C motif chemokine ligand 12 ( Cxcl12) , and of inflammatory cytokines, revealed that αPD-L1 treatment reduced their expression, while blocking CCR2 reversed this effect. Conclusions The CCR2/CCL2 axis is required to modify pathology using PD-L1 blockade in a mouse model of tauopathy. This modification involves, in addition to monocytes, the accumulation of FOXP3 + regulatory CD4 + T cells in the brain, and the T-cell chemoattractant, Cxcl12 .

Survival of larval Antarctic krill (Euphausia superba) during winter is largely dependent upon the presence of sea ice as it provides an important source of food and shelter. We hypothesized that sea ice provides additional benefits because it hosts fewer competitors and provides reduced predation risk for krill larvae than the water column. To test our hypothesis, zooplankton were sampled in the Weddell-Scotia Confluence Zone at the ice-water interface (0–2 m) and in the water column (0–500 m) during August–October 2013. Grazing by mesozooplankton, expressed as a percentage of the phytoplankton standing stock, was higher in the water column (1.97 ± 1.84%) than at the ice-water interface (0.08 ± 0.09%), due to a high abundance of pelagic copepods. Predation risk by carnivorous macrozooplankton, expressed as a percentage of the mesozooplankton standing stock, was significantly lower at the ice-water interface (0.83 ± 0.57%; main predators amphipods, siphonophores and ctenophores) than in the water column (4.72 ± 5.85%; main predators chaetognaths and medusae). These results emphasize the important role of sea ice as a suitable winter habitat for larval krill with fewer competitors and lower predation risk. These benefits should be taken into account when considering the response of Antarctic krill to projected declines in sea ice. Whether reduced sea-ice algal production may be compensated for by increased water column production remains unclear, but the shelter provided by sea ice would be significantly reduced or disappear, thus increasing the predation risk on krill larvae.

Protective immunity, essential for brain maintenance and repair, may be compromised in Alzheimer’s disease (AD). Here, using high-dimensional single-cell mass cytometry, we find a unique immunometabolic signature in circulating CD4 + T cells preceding symptom onset in individuals with familial AD, featured by the elevation of CD38 expression. Using female 5xFAD mice, a mouse model of AD, we show that treatment with an antibody directed to CD38 leads to restored metabolic fitness, improved cognitive performance, and attenuated local neuroinflammation. Comprehensive profiling across distinct immunological niches in 5xFAD mice, reveals a high level of disease-associated CD4 + T cells that produce IL-17A in the dural meninges, previously linked to cognitive decline. Targeting CD38 leads to abrogation of meningeal T H 17 immunity and cortical IL-1β, breaking the negative feedback loop between these two compartments. Taken together, the present findings suggest CD38 as an immunometabolic checkpoint that could be adopted as a pre-symptomatic biomarker for early diagnosis of AD, and might also be therapeutically targeted alone or in combination with other immunotherapies for disease modification. Maladaptive immunity negatively impacts Alzheimer’s disease (AD). Here, the authors show dysfunctional CD38-expressing CD4 +  T cells in individuals with familial AD before symptom onset. Targeting CD38 in an AD mouse model restored metabolic fitness, improved cognition, and modified meningeal immunity.

Arctic cod (Boreogadus saida) is the most abundant forage fish in the Arctic Ocean. Here we review Arctic cod habitats, distribution, ecology, and physiology to assess how climate change and other anthropogenic stressors are affecting this key species. This review identifies vulnerabilities for different life stages across the entire distribution range of Arctic cod. We explore the impact of environmental (abiotic and biotic) and anthropogenic stressors on Arctic cod with a regional perspective in a scenario up to the year 2050 and identify knowledge gaps constraining predictions. Epipelagic eggs and larvae are more vulnerable to climate change and stressors than adults. Increased water temperatures, sea-ice decline, altered freshwater input, acidification, changing prey field, increased interspecific competition, new predators, and pollution are the principal stressors that will affect Arctic cod populations. Detrimental effects are likely to be greater in regions characterized by the advection of warmer Atlantic and Pacific waters. In contrast, Arctic cod may benefit from ocean warming in colder areas of the High Arctic. The risk from fisheries is moderate and primarily limited to bycatch. Overall, a decrease in suitable habitat and an associated decline in total Arctic cod biomass are predicted. In most Arctic seas, the relative abundance of Arctic cod within the fish community will likely fluctuate in accordance with cold and warm periods. A reduced abundance of Arctic cod will negatively affect the abundance, distribution, and physiological condition of certain predators, whereas some predators will successfully adapt to a more boreal diet. Regional management measures that recognize the critical role of Arctic cod are required to ensure that increased anthropogenic activities do not exacerbate the impacts of climate change on Arctic marine ecosystems. Ultimately, the mitigation of habitat loss for Arctic cod will only be achieved through a global reduction in carbon emissions.

Arctic sea ice is highly heterogeneous and composed of a mosaic of different habitats. Our understanding of the impact of climate change on Arctic sea ice and especially on the ice-associated ecosystems is hindered by both a lack of data and a limited understanding of the processes associated with different sea-ice habitats. In particular sea-ice ridges are one of the most under-sampled and poorly understood components of the Arctic sea-ice system. During a spring campaign in the Arctic Ocean, we combined a number of sampling approaches to quantify: 1) the spatial variability of sea-ice algae at single floe and multiple floe scales; 2) the contribution of ridges to ice algal spatial variability; and 3) the role of ridges in shaping the sea ice as a habitat. For upscaling purposes, algal biomass retrieved from ice cores was compared with biomass estimates based on under-ice profiles covering a total of 36 km. Our results show that the level-ice spatial variability measured on a single ice floe can be representative of the larger scale variability. However, only when ridges are included in the analysis we are able to obtain a comprehensive picture of the large-scale ice algal biomass variability. In spring, ridges let more light pass through the ice due to their geometry and their effects on snow distribution, they thus offer a potentially favorable environment for algae to grow within, and they can act as funnels of light for pelagic organisms. On a large scale, ridges contribute more than 50% percent of the potential habitable space for ice algae for snow-covered Arctic sea ice in spring.