BIS-guided anesthesia reduced anesthetic exposure and decreased the risk of POCD at 3 months after surgery. For every 1000 elderly patients undergoing major surgery, anesthetic delivery titrated to a range of BIS between 40 and 60 would prevent 23 patients from POCD and 83 patients from delirium.

Adiponectin (ADN) is an adipocyte-secreted protein with insulinsensitizing, antidiabetic, antiinflammatory, and antiatherogenic properties. Evidence is also accumulating that ADN has neuroprotective activities, yet the underlying mechanism remains elusive. Here we show that ADN could pass through the bloodbrain barrier, and elevating its levels in the brain increased cell proliferation and decreased depression-like behaviors. ADN deficiency did not reduce the basal hippocampal neurogenesis or neuronal differentiation but diminished the effectiveness of exercise in increasing hippocampal neurogenesis. Furthermore, exerciseinduced reduction in depression-like behaviors was abrogated in ADN-deficient mice, and this impairment in ADN-deficient mice was accompanied by defective running-induced phosphorylation of AMP-activated protein kinase (AMPK) in the hippocampal tissue. In vitro analyses indicated that ADN itself could increase cell proliferation of both hippocampal progenitor cells and Neuro2a neuroblastoma cells. The neurogenic effects of ADN were mediated by the ADN receptor 1 (ADNR1), because siRNA targeting ADNR1, but not ADNR2, inhibited the capacity of ADN to enhance cell proliferation. These data suggest that adiponectin may play a significant role in mediating the effects of exercise on hippocampal neurogenesis and depression, possibly by activation of the ADNR1/AMPK signaling pathways, and also raise the possibility that adiponectin and its agonists may represent a promising therapeutic treatment for depression.adiponectin | adiponectin receptor | physical exercise | hippocampal neurogenesis | depression-like behavior

Background The coronavirus disease 2019 (COVID-19) pandemic is having a profound impact on the health and development of children worldwide. There is limited evidence on the impact of COVID-19 and its related school closures and disease-containment measures on the psychosocial wellbeing of children; little research has been done on the characteristics of vulnerable groups and factors that promote resilience. Methods We conducted a large-scale cross-sectional population study of Hong Kong families with children aged 2–12 years. Parents completed an online survey on family demographics, child psychosocial wellbeing, functioning and lifestyle habits, parent–child interactions, and parental stress during school closures due to COVID-19. We used simple and multiple linear regression analyses to explore factors associated with child psychosocial problems and parental stress during the pandemic. Results The study included 29,202 individual families; of which 12,163 had children aged 2–5 years and 17,029 had children aged 6–12 years. The risk of child psychosocial problems was higher in children with special educational needs, and/or acute or chronic disease, mothers with mental illness, single-parent families, and low-income families. Delayed bedtime and/or inadequate sleep or exercise duration, extended use of electronic devices were associated with significantly higher parental stress and more psychosocial problems among pre-schoolers. Conclusions This study identifies vulnerable groups of children and highlights the importance of strengthening family coherence, adequate sleep and exercise, and responsible use of electronic devices in promoting psychosocial wellbeing during the COVID-19 pandemic. Electronic supplementary material The online version of this article (10.1007/s00787-020-01680-8) contains supplementary material, which is available to authorized users.

An influential hypothesis from the last decade proposed that regions within the right inferior frontal cortex of the human brain were dedicated to supporting response inhibition. There is growing evidence, however, to support an alternative model, which proposes that neural areas associated with specific inhibitory control tasks co-exist as common network mechanisms, supporting diverse cognitive processes. This meta-analysis of 225 studies comprising 323 experiments examined the common and distinct neural correlates of cognitive processes for response inhibition, namely interference resolution, action withholding, and action cancellation. Activation coordinates for each subcategory were extracted using multilevel kernel density analysis (MKDA). The extracted activity patterns were then mapped onto the brain functional network atlas to derive the common (i.e., process-general) and distinct (i.e., domain-oriented) neural network correlates of these processes. Independent of the task types, activation of the right hemispheric regions (inferior frontal gyrus, insula, median cingulate, and paracingulate gyri) and superior parietal gyrus was common across the cognitive processes studied. Mapping the activation patterns to a brain functional network atlas revealed that the fronto-parietal and ventral attention networks were the core neural systems that were commonly engaged in different processes of response inhibition. Subtraction analyses elucidated the distinct neural substrates of interference resolution, action withholding, and action cancellation, revealing stronger activation in the ventral attention network for interference resolution than action inhibition. On the other hand, action withholding/cancellation primarily engaged the fronto-striatal circuit. Overall, our results suggest that response inhibition is a multidimensional cognitive process involving multiple neural regions and networks for coordinating optimal performance. This finding has significant implications for the understanding and assessment of response inhibition.Electronic supplementary materialThe online version of this article (doi:10.1007/s00429-017-1443-x) contains supplementary material, which is available to authorized users.

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Summary:Purpose: Memory deficits in epileptic patients have been found in some, but not all studies assessing the effects of side of seizures and resection from a temporal lobe on cognitive performance. The purpose of this study was to provide a quantitative review of previous studies on this issue.Methods: Based on conventional meta-analytic procedures, we identified 33 studies that assessed verbal and nonverbal memory performance before and after anterior temporal lobectomy. The Logical Memory and Visual Reproduction subtests from the Wechsler Memory Scale were used. These studies were then subjected to two levels of analyses: (a) vote-counting procedure, and (b) effect-size calculations and comparisons.Results: Overall, the data confirmed previous findings that verbal memory tasks are sensitive to left hemisphere dysfunction. The efficacy of a "nonverbal" task for tapping function in the nondominant (right) hemisphere was not confirmed, although a trend supporting this speculation was observed. With regard to the comparison of changes in verbal and nonverbal memory before and after resection from a temporal lobe, a clear trend was observed for decline in verbal memory function after resection from the left, especially significant for immediate verbal recall. A trend for contralateral improvement on nonverbal memory also was observed. The pattern of memory change after resection from the right temporal lobe was less clear.Conclusions: The findings of this study suggest that side of epileptic seizure and surgical resection from a temporal lobe affect verbal memory functions. The relations between the laterality of epileptic seizure, surgical resection from the temporal lobe, and nonverbal memory are to be verified by further research.

The accurate detection of deception or lying is a challenge to experts in many scientific disciplines. To investigate if specific cerebral activation characterized feigned memory impairment, six healthy male volunteers underwent functional magnetic resonance imaging with a block-design paradigm while they performed forced-choice memory tasks involving both simulated malingering and under normal control conditions. Malingering that demonstrated the existence and involvement of a prefrontal-parietal-sub-cortical circuit with feigned memory impairment produced distinct patterns of neural activation. Because astute liars feign memory impairment successfully in testing once they understand the design of the measure being employed, our study represents an extremely significant preliminary step towards the development of valid and sensitive methods for the detection of deception.

Exercise promotes hippocampal neurogenesis and dendritic plasticity while stress shows the opposite effects, suggesting a possible mechanism for exercise to counteract stress. Changes in hippocampal neurogenesis and dendritic modification occur simultaneously in rats with stress or exercise; however, it is unclear whether neurogenesis or dendritic remodeling has a greater impact on mediating the effect of exercise on stress since they have been separately examined. Here we examined hippocampal cell proliferation in runners treated with different doses (low: 30 mg/kg; moderate: 40 mg/kg; high: 50 mg/kg) of corticosterone (CORT) for 14 days. Water maze task and forced swim tests were applied to assess hippocampal-dependent learning and depression-like behaviour respectively the day after the treatment. Repeated CORT treatment resulted in a graded increase in depression-like behaviour and impaired spatial learning that is associated with decreased hippocampal cell proliferation and BDNF levels. Running reversed these effects in rats treated with low or moderate, but not high doses of CORT. Using 40 mg/kg CORT-treated rats, we further studied the role of neurogenesis and dendritic remodeling in mediating the effects of exercise on stress. Co-labelling with BrdU (thymidine analog) /doublecortin (immature neuronal marker) showed that running increased neuronal differentiation in vehicle- and CORT-treated rats. Running also increased dendritic length and spine density in CA3 pyramidal neurons in 40 mg/kg CORT-treated rats. Ablation of neurogenesis with Ara-c infusion diminished the effect of running on restoring spatial learning and decreasing depression-like behaviour in 40 mg/kg CORT-treated animals in spite of dendritic and spine enhancement. but not normal runners with enhanced dendritic length. The results indicate that both restored hippocampal neurogenesis and dendritic remodelling within the hippocampus are essential for running to counteract stress.