Hot metacognition: poorer metacognitive efficiency following acute but not traumatic stress.

Aberrations to metacognition-the ability to reflect on and evaluate self-performance-are a feature of poor mental health. Theoretical models of post-traumatic stress disorder propose that following severe stress or trauma, maladaptive metacognitive evaluations and appraisals of the event drive the development of symptoms. Empirical research is required in order to reveal whether disruptions to metacognition cause or contribute to symptom development in line with theoretical accounts, or are simply a consequence of ongoing psychopathology.

Early-life stress biases responding to negative feedback and increases amygdala volume and vulnerability to later-life stress.

Early-life stress (ELS) or adversity, particularly in the form of childhood neglect and abuse, is associated with poor mental and physical health outcomes in adulthood. However, whether these relationships are mediated by the consequences of ELS itself or by other exposures that frequently co-occur with ELS is unclear. To address this question, we carried out a longitudinal study in rats to isolate the effects of ELS on regional brain volumes and behavioral phenotypes relevant to anxiety and depression.

Genetic variants associated with psychiatric disorders are enriched at epigenetically active sites in lymphoid cells.

Multiple psychiatric disorders have been associated with abnormalities in both the innate and adaptive immune systems. The role of these abnormalities in pathogenesis, and whether they are driven by psychiatric risk variants, remains unclear. We test for enrichment of GWAS variants associated with multiple psychiatric disorders (cross-disorder or trans-diagnostic risk), or 5 specific disorders (cis-diagnostic risk), in regulatory elements in immune cells.

Methylome-wide association study of antidepressant use in Generation Scotland and the Netherlands Twin Register implicates the innate immune system.

Antidepressants are an effective treatment for major depressive disorder (MDD), although individual response is unpredictable and highly variable. Whilst the mode of action of antidepressants is incompletely understood, many medications are associated with changes in DNA methylation in genes that are plausibly linked to their mechanisms. Studies of DNA methylation may therefore reveal the biological processes underpinning the efficacy and side effects of antidepressants.

Dysconnectivity of a brain functional network was associated with blood inflammatory markers in depression.

Objective: There is increasing evidence for a subgroup of major depressive disorder (MDD) associated with heightened peripheral blood inflammatory markers. In this study, we aimed to understand the mechanistic brain-immune axis in inflammation-linked depression by investigating associations between functional connectivity (FC) of brain networks and peripheral blood immune markers in depression.

Methods: Resting-state functional magnetic resonance imaging (fMRI) and peripheral blood inflammatory markers (C-reactive protein; CRP, interleukin-6; IL-6 and immune cells) were collected on N = 46 healthy controls (HC; CRP ≤ 3 mg/L) and N = 83 cases of depression, stratified further into low CRP cases (loCRP cases; ≤ 3 mg/L; N = 50) and high CRP cases (hiCRP cases; > 3 mg/L; N = 33).

B-cells are abnormal in psychosocial stress and regulate meningeal myeloid cell activation.

There is increasing interest in how immune cells, including those within the meninges at the blood-brain interface, influence brain function and mood disorders, but little data on humoral immunity in this context. Here, we show that in mice exposed to psychosocial stress, there is increased splenic B cell activation and secretion of the immunoregulatory cytokine interleukin (IL)-10. Meningeal B cells were prevalent in homeostasis but substantially decreased following stress, whereas Ly6C monocytes increased, and meningeal myeloid cells showed augmented expression of activation markers.

No evidence for differential gene expression in major depressive disorder PBMCs, but robust evidence of elevated biological ageing.

The increasingly compelling data supporting the involvement of immunobiological mechanisms in Major Depressive Disorder (MDD) might provide some explanation forthe variance in this heterogeneous condition. Peripheral blood measures of cytokines and chemokines constitute the bulk of evidence, with consistent meta-analytic data implicating raised proinflammatory cytokines such as IL6, IL1β and TNF. Among the potential mechanisms linking immunobiological changes to affective neurobiology is the accelerated biological ageing seen in MDD, particularly via the senescence associated secretory phenotype (SASP).

Early-life stress and inflammation: A systematic review of a key experimental approach in rodents.

Repeated maternal separation is the most widely used pre-clinical approach to investigate the relationship between early-life chronic stress and its neuropsychiatric and physical consequences. In this systematic review, we identified 46 studies that conducted repeated maternal separation or single-episode maternal separation and reported measurements of interleukin-1b, interleukin-6, interleukin-10, tumour necrosis factor-alpha, or microglia activation and density. We report that in the short-term and in the context of later-life stress, repeated maternal separation has pro-inflammatory immune consequences in diverse tissues.

Inflammatory and cardiometabolic markers at presentation with first episode psychosis and long-term clinical outcomes: A longitudinal study using electronic health records.

Approximately one third of patients presenting with a first episode of psychosis need long-term support, but there is a limited understanding of the sociodemographic or biological factors that predict this outcome. We used electronic health records from a naturalistic cohort of consecutive patients referred to an early intervention in psychosis service to address this question. We extracted data on demographic (age, sex, ethnicity and marital status), immune (differential cell count measures and C-reactive protein (CRP)) and metabolic (cholesterol, triglycerides, glucose, glycated haemoglobin, blood pressure, body mass index (BMI)) factors at baseline, and subsequent need for long-term secondary (specialist) psychiatric care.

Peripheral Blood Cell-Stratified Subgroups of Inflamed Depression.

Background: Depression has been associated with increased inflammatory proteins, but changes in circulating immune cells are less well defined.

Methods: We used multiparametric flow cytometry to count 14 subsets of peripheral blood cells in 206 depression cases and 77 age- and sex-matched controls (N = 283). We used univariate and multivariate analyses to investigate the immunophenotypes associated with depression and depression severity.

Detection of functional brain network reconfiguration during task-driven cognitive states.

Network science offers computational tools to elucidate the complex patterns of interactions evident in neuroimaging data. Recently, these tools have been used to detect dynamic changes in network connectivity that may occur at short time scales. The dynamics of fMRI connectivity, and how they differ across time scales, are far from understood.

Cognitive network neuroscience.

Network science provides theoretical, computational, and empirical tools that can be used to understand the structure and function of the human brain in novel ways using simple concepts and mathematical representations. Network neuroscience is a rapidly growing field that is providing considerable insight into human structural connectivity, functional connectivity while at rest, changes in functional networks over time (dynamics), and how these properties differ in clinical populations. In addition, a number of studies have begun to quantify network characteristics in a variety of cognitive processes and provide a context for understanding cognition from a network perspective.

Brain network adaptability across task states.

Activity in the human brain moves between diverse functional states to meet the demands of our dynamic environment, but fundamental principles guiding these transitions remain poorly understood. Here, we capitalize on recent advances in network science to analyze patterns of functional interactions between brain regions. We use dynamic network representations to probe the landscape of brain reconfigurations that accompany task performance both within and between four cognitive states: a task-free resting state, an attention-demanding state, and two memory-demanding states.

Functional connectivity and brain networks in schizophrenia.

Schizophrenia has often been conceived as a disorder of connectivity between components of large-scale brain networks. We tested this hypothesis by measuring aspects of both functional connectivity and functional network topology derived from resting-state fMRI time series acquired at 72 cerebral regions over 17 min from 15 healthy volunteers (14 male, 1 female) and 12 people diagnosed with schizophrenia (10 male, 2 female). We investigated between-group differences in strength and diversity of functional connectivity in the 0.