The costs of coping: Different strategies to deal with social defeat stress might come with distinct immunologic, neuroplastic, and oxidative stress consequences in male Wistar rats.

The impact of stress on health and well-being is determined by the ability of an individual to cope with challenges imposed by the stressor. Animals exposed to social defeat stress show different patterns of response during confrontations, leading to distinct stress-induced consequences. Using an established resident-intruder paradigm, we explored the outcomes of adopting active or passive coping strategies during a social defeat protocol over peripheral and central nervous system (CNS) levels of inflammatory cytokines, growth factors, glucocorticoid, and oxidative stress markers in male Wistar rats.

Reduction of hippocampal IL-6 levels in LPS-injected rats following acute exendin-4 treatment.

Preclinical evidence on the role of glucagon-like peptide-1 receptor (GLP-1r) agonists in the brain led to an increased interest in repurposing these compounds as a therapy for central nervous system (CNS) disorders and associated comorbidities. We aimed to investigate the neuroprotective effects of acute treatment with exendin (EX)-4, a GLP-1r agonist, in an animal model of inflammation. We evaluated the effect of different doses of EX-4 on inflammatory, neurotrophic, and oxidative stress parameters in the hippocampus and serum of lipopolysaccharide (LPS)-injected animals.

Anhedonic-like behavior correlates with IFNγ serum levels in a two-hit model of depression.

Stress is implicated in the etiology of major depressive disorder (MDD) and leads to the activation of proinflammatory pathways, which are recognized to induce depressive symptoms. For instance, depression is commonly observed in patients with hepatitis C and cancer under IFN therapy, and high levels of inflammatory cytokines are described in the serum of individuals with MDD - which indicate a multi-system aspect of psychiatric disorders. Thus, we evaluated the effects of a two-hit model of depression on peripheral and CNS inflammatory, neurotrophic, and oxidative stress parameters and behavior.

DNA methylation in adolescents with anxiety disorder: a longitudinal study.

Anxiety disorders (AD) typically manifest in children and adolescents and might persist into adulthood. However, there are still few data concerning epigenetic mechanisms associated with onset, persistence or remission of AD over time. We investigated a cohort of adolescents and young adults at baseline (age; 13.

Oxidative stress markers imbalance in late-life depression.

Background: Oxidative stress has been implicated in the pathophysiology of mood disorders in young adults. However, there is few data to support its role in the elderly. The primary aim of this study was to evaluate whether subjects with late-life depression (LLD) presented with changes in oxidative stress response in comparison with the non-depressed control group.

Reduced serum concentrations of brain-derived neurotrophic factor (BDNF) in transsexual Brazilian men.

Serum BDNF levels are significantly decreased in transsexual Brazilian women when compared to cis-sexual men. Since transsexual men are also exposed to chronic social stress and have a high prevalence of associated psychopathologies, it is plausible to inquire if BDNF serum levels are altered in transsexual men as well. Therefore, our objective was to evaluate differences in BDNF serum level of transsexual men when compared to cis-sexual men and women.

Telomere length in subjects with schizophrenia, their unaffected siblings and healthy controls: Evidence of accelerated aging.

Schizophrenia (SZ) is associated with broad burden. The clinical manifestations of SZ are related to pathophysiological alterations similar to what is seen in normal aging. Our aim was to evaluate the differences in telomere length (TL), a biomarker of cellular aging, in subjects with SZ (n=36), unaffected siblings (SB, n=36) and healthy controls (HC, n=47).

What can HPA axis-linked genes tell us about anxiety disorders in adolescents?

Introduction: Anxiety disorders (AD) share features of both anxiety and fear linked to stress response. The hypothalamic-pituitary-adrenal (HPA) axis is considered the core biological pathway of the stress system and it is known that an inappropriate response to environmental stimuli may be related to individual genetic vulnerability in HPA-linked genes. Despite the biological plausibility of a relationship between the HPA axis and AD, few studies have investigated associations between genetic polymorphisms linked to the HPA axis and this complex disorder.

Could BDNF be involved in compensatory mechanisms to maintain cognitive performance despite acute sleep deprivation? An exploratory study.

Background: Neuroimaging studies suggest that acute sleep deprivation can lead to adaptations, such as compensatory recruitment of cerebral structures, to maintain cognitive performance despite sleep loss. However, the understanding of the neurochemical alterations related to these adaptations remains incomplete.

Objective: Investigate BDNF levels, cognitive performance and their relations in healthy subjects after acute sleep deprivation.

Mineralocorticoid receptor genotype moderates the association between physical neglect and serum BDNF.

The objective of this study is to investigate if a polymorphism in the NR3C2 gene moderates the association between childhood trauma on serum levels of brain derived neurothrophic factor (sBDNF). sBDNF was used here as a general marker of alteration in brain function. This is a community cross sectional study comprising 90 adolescents (54 with anxiety disorders).