Moderating effect of insulin resistance on the relationship between cortical surface area and cognitive function in patients with first-episode schizophrenia.

Objective: The mechanisms underlying cognitive deficits in schizophrenia remain unclear. Accumulating evidence suggests that insulin resistance (IR) is closely related to brain structure and cognitive impairment. We aimed to determine whether IR mediates or moderates the association between cortical surface area (CSA) and cognitive function in patients with first-episode schizophrenia (PFES).

Immunosenescence-related T cell phenotypes, structural brain imaging, and cognitive impairment in patients with schizophrenia: a moderated mediation analysis.

Cognitive impairment is a core characteristic of schizophrenia. Immunosenescence has been consistently implicated in the cognitive dysfunction observed in neurodegenerative diseases, but how it may relate to cognitive deficits in schizophrenia is still unclear. We explored the associations between immunosenescence and cognitive impairment in patients with schizophrenia (SCZ, n = 65) and healthy controls (HCs, n = 39).

Serum kynurenine metabolites and cytokine levels: diagnostic and predictive implications in acute manic episodes of bipolar disorder.

In this study, we aimed to integrate serum cytokine and kynurenine metabolite levels to identify key biomarkers for diagnosing and predicting treatment outcomes in bipolar disorder during manic episodes (BDM). A total of 52 patients with BDM and 49 healthy controls (HCs) were recruited. Serum levels of cytokines and kynurenine metabolites were measured at baseline.

Cortisol response patterns to stress correlated to white matter integrity and duration of illness in patients with schizophrenia.

Stress plays a critical role in schizophrenia pathogenesis, and blunted cortisol responses to acute stress exposure among patients with schizophrenia may be related to damaged white matter (WM) fibers in specific brain regions. The present aim was to assess correlations between cortisol response patterns and changes in WM integrity in patients with schizophrenia and to determine if such changes relate to the duration of illness. This study included patients with chronic schizophrenia (PCS, n = 92), patients with first-episode schizophrenia (PFS, n = 86), and healthy controls (HC, n = 77).

Immunosenescence-related T cell phenotypes and white matter in schizophrenia patients with tardive dyskinesia.

Schizophrenia patients with tardive dyskinesia (TD) are associated with accelerated biological aging, immunological dysfunction, and premature morbidity and mortality. Older individuals are particularly vulnerable to TD development. As a characteristic of immunosenescence, alterations in the relative proportions of naïve or memory T cell subpopulations may be negatively or positively associated with brain structure abnormalities; however, whether these changes are correlated with TD remains unclear.

Serum neuroactive metabolites of the tryptophan pathway in patients with acute phase of affective disorders.

Background: Many studies showed disrupted tryptophan metabolism in patients with affective disorders. The aims of this study were to explore the differences in the metabolites of tryptophan pathway (TP) and the relationships between TP metabolites and clinical symptoms, therapeutic effect in patients with bipolar disorder with acute manic episode (BD-M), depressive episode (BD-D) and major depressive disorder (MDD).

Methods: Patients with BD-M (n=52) and BD-D (n=39), MDD (n=48) and healthy controls (HCs, n=49) were enrolled.

Role of the immune-kynurenine pathway in treatment-resistant schizophrenia.

Background: The immune-inflammatory response system (IRS) and kynurenine pathway (KP) have been implicated in the pathophysiology of schizophrenia. Studies have shown inflammation-related effects on KP metabolism in patients with schizophrenia. This study investigated the relationship between KP metabolites, IRS, and the compensatory immune-regulatory reflex system (CIRS) in patients with treatment-resistant schizophrenia (TRS).

Correlation of Immune-Inflammatory Response System (IRS)/Compensatory Immune-Regulatory Reflex System (CIRS) with White Matter Integrity in First-Episode Patients with Schizophrenia.

Several studies have reported compromised white matter integrity, and that some inflammatory mediators may underlie this functional dysconnectivity in the brain of patients with schizophrenia. The immune-inflammatory response system and compensatory immune-regulatory reflex system (IRS/CIRS) are novel biomarkers for exploring the role of immune imbalance in the pathophysiological mechanism of schizophrenia. This study aimed to explore the little-known area regarding the composite score of peripheral cytokines, the IRS/CIRS, and its correlation with white matter integrity and the specific microstructures most affected in schizophrenia.

Replenished microglia partially rescue schizophrenia-related stress response.

Background: Microglia play an important role in the maintenance of brain and behavioral homeostasis. The protective effect of microglial replenishment was reported in neurological diseases, but whether microglial therapy would benefit psychiatric disorders such as schizophrenia has been unclear. As schizophrenia is a stress-vulnerable disorder and psychosocial stress promotes inflammation and microglial activation, we aim to understand how microglial replenishment works in stress-associated schizophrenia.

CSF1R regulates schizophrenia-related stress response and vascular association of microglia/macrophages.

Background: Microglia are known to regulate stress and anxiety in both humans and animal models. Psychosocial stress is the most common risk factor for the development of schizophrenia. However, how microglia/brain macrophages contribute to schizophrenia is not well established.

Immune-Inflammatory Response And Compensatory Immune-Regulatory Reflex Systems And White Matter Integrity in Schizophrenia.

Background And Hypothesis: Low-grade neural and peripheral inflammation are among the proposed pathophysiological mechanisms of schizophrenia. White matter impairment is one of the more consistent findings in schizophrenia but the underlying mechanism remains obscure. Many cerebral white matter components are sensitive to neuroinflammatory conditions that can result in demyelination, altered oligodendrocyte differentiation, and other changes.

Inflammatory disequilibrium and lateral ventricular enlargement in treatment-resistant schizophrenia.

Treatment-resistant schizophrenia (TRS) patient respond poorly to antipsychotics. Inflammatory imbalance involving pro- and anti-inflammatory cytokines may play an important role in the mechanism of antipsychotic-medication response. This study aimed to investigate immune imbalance and how the latter relates to clinical manifestations in patients with TRS.

Glial receptor PLXNB2 regulates schizophrenia-related stress perception the amygdala.

Stress is a trigger for the development of psychiatric disorders. However, how stress trait differs in schizophrenia patients is still unclear. Stress also induces and exacerbates immune activation in psychiatric disorders.

Alterations in innate immune defense distinguish first-episode schizophrenia patients from healthy controls.

Innate immune components involved in host defense have been implicated in schizophrenia (SCZ). However, studies exploring their clinical utility in SCZ diagnosis are limited. The main purpose of this study was to evaluate whether circulating endotoxin, high mobility group box 1 protein (HMGB1) and complement component 4 (C4) could act as peripheral biomarkers to distinguish first-episode schizophrenia (FES, = 42) patients from healthy controls (HCs, = 35) in associations with psychopathological symptoms and cognitive dysfunctions.

The relationship between TLR4/NF-κB/IL-1β signaling, cognitive impairment, and white-matter integrity in patients with stable chronic schizophrenia.

Objective: Previous studies have implicated intricate interactions between innate immunity and the brain in schizophrenia. Monocytic Toll-like receptor (TLR) 4 signaling, a crucial "sensor" of innate immunity, was reported to be over-activated in link with cognitive impairment in schizophrenia. As TLR4 is predominantly expressed on gliocytes prior to expression in neurons, we hypothesized that higher TLR4 levels may contribute to cognitive deterioration by affecting white matter microstructure.

Serum hyperhomocysteine and cognitive impairment in first-episode patients with schizophrenia: Moderated by brain cortical thickness.

The mechanism by which high homocysteine (HCY) may aggravate cognitive impairment in patients with schizophrenia is not well understood. We aimed to test the hypothesis that hyperhomocysteinaemia may exacerbate cognitive deficits by mediating the decrease in cortical thickness in patients with schizophrenia. One hundred and sixty-seven first-episode patients with schizophrenia (FEPS) and 120 healthy controls (HCs) were included.

Kynurenine metabolism and metabolic syndrome in patients with schizophrenia.

Accumulating evidence indicates that a dysregulated kynurenine (KYN) pathway (KP) metabolism may play an important role in the pathogenesis of both schizophrenia and metabolic syndrome (MS). However, the underlying mechanisms remain poorly understood. Here, we aimed to evaluate the potential roles of KP in the pathogenesis of MS in schizophrenia.

Effects of microRNA-181b-5p on cognitive deficits in first-episode patients with schizophrenia: Mediated by BCL-2.

MicroRNA (miR)-181b-5p is considered to be involved in the pathogenesis of schizophrenia, and one of its regulatory target genes BCL-2 (B-cell lymphoma 2) is suggested to associate with cognition of schizophrenia. Cognitive deficit is a core trait of schizophrenia. However, it remains unclear whether miR-181b-5p affects cognition and its possible pathway in schizophrenia.

Allostatic Load Effects on Cortical and Cognitive Deficits in Essentially Normotensive, Normoweight Patients with Schizophrenia.

Reduced cortical gray matter integrity and cognitive abilities are among core deficits in schizophrenia. We hypothesized that higher allostatic load (AL) that accounts for exposure to chronic stress is a contributor to structural and cognitive deficits in schizophrenia. One hundred and sixty-seven schizophrenia patients who were on average with normal weight, normal systolic, and diastolic blood pressure and 72 healthy controls were enrolled in the study.

Genome-wide DNA methylation analysis of peripheral blood cells derived from patients with first-episode schizophrenia in the Chinese Han population.

Schizophrenia is a severe neuropsychiatric disorder with core features including hallucinations, delusions, and cognition deficits. Accumulating evidence has implicated abnormal DNA methylation in the development of schizophrenia. However, the mechanisms by which DNA methylation changes alter the risk for schizophrenia remain largely unknown.