Neurohumoral markers that predict the efficiency of pharmacologic therapy of depressive disorders

We present a comprehensive clinical and biological study of 46 patients with depressive disorder (F32-F33: depressive episode and recurrent depressive disorder) during pharmacotherapy. Neurohumoral factors (cortisol, brain-derived neurotrophic factor, serotonin, DHEA and its sulfated form) were determined in serum by ELISA. The severity of the current depressive episode was evaluated using the 17-point Hamilton Depression Rating Scale (HDRS-17); the pharmacotherapy efficacy was evaluated using the scale of the Clinical Global Impression (CGI Scale). We showed that before prescription of pharmacotherapy peripheral blood neurohumoral markers that characterize the state of stress-realizing and stress-limiting systems of the body may be considered as biological predictors of the effective pharmacotherapy of a current depressive episode and used as additional paraclinical examination methods. At higher concentrations of cortisol and serotonin associated with a decrease in the content of neurosteroid dehydroepiandrosterone, the high efficiency of the pharmacotherapy of depressive episode is predicted

Glutamate Concentration in the Serum of Patients with Schizophrenia

Glutamate is the major neurotransmitter with multiple functions in the central nervous system. Glutamate-mediated excitotoxicity is involved in the pathophysiological processes in schizophrenia. The purpose of this study was to determine the concentration of glutamate in the serum of patients with paranoid schizophrenia compared with healthy individuals, and depending on the duration of the schizophrenic process and leading clinical symptoms. We investigated the level of glutamate in the serum of 158 patients with paranoid schizophrenia and 94 healthy persons. Higher concentrations of glutamate in schizophrenic patients compared with healthy persons have been found. The maximum concentrations of glutamate were detected in patients with disease duration of more than ten years. Glutamate level in the serum does not depend on the prevailing negative or positive clinical symptoms. The increased concentration of glutamate can hypothetically contribute to dopaminergic and glutamatergic imbalance, leading to the development of psychotic symptoms and cognitive dysfunction

EEG alpha band characteristics in patients with a depressive episode within recurrent and bipolar depression

BACKGROUND: The search for biological markers for the differential diagnosis of recurrent depression and bipolar depression is an important undertaking in modern psychiatry. Electroencephalography (EEG) is one of the promising tools in addressing this challenge. AIM: To identify differences in the quantitative characteristics of the electroencephalographic alpha band activity in patients with a depressive episode within the framework of recurrent depression and bipolar depression. METHODS: Two groups of patients (all women) were formed: one consisting of subjects with recurrent depressive disorder and one with subjects experiencing a current mild/moderate episode (30 patients), and subjects with bipolar affective disorder or a current episode of mild or moderate depression (30 patients). The groups did not receive pharmacotherapy and did not differ in their socio-demographic parameters or total score on the Hamilton depression scale. A baseline electroencephalogram was recorded, and the quantitative characteristics of the alpha band activity were analyzed, including the absolute spectral power, interhemispheric coherence, and EEG activation. RESULTS: The patients with recurrent depressive disorder demonstrated statistically significantly lower values of the average absolute spectral power of the alpha band (z=2.481; p=0.042), as well as less alpha attenuation from eyes closed to eyes open (z=2.573; p=0.035), as compared with the patients with bipolar affective disorder. CONCLUSION: The presented quantitative characteristics of alpha activity are confirmation that patients with affective disorders of different origins also display distinctive electrophysiological features which can become promising biomarkers and could help separate bipolar depression from the recurrent type

Study of early onset schizophrenia:Associations of GRIN2A and GRIN2B polymorphisms

Background: Schizophrenia is a complex mental disorder with a high heritability. Dysfunction of the N-methyl-D-aspartate (NMDA)-type glutamate receptors may be involved in the pathogenesis of schizophrenia. In this study, we examined the contribution of GRIN2A and GRIN2B (Glutamate Ionotropic Receptor NMDA Type Subunit 2A/2B) polymorphisms to the clinical features of schizophrenia, such as the leading symptoms, the type of course, and the age of onset. Methods: A population of 402 Russian patients with schizophrenia from the Siberian region was investigated. Genotyping of seventeen single-nucleotide polymorphisms (SNPs) in GRIN2A and GRIN2B was performed using QuantStudio™ 3D Digital PCR System Life Technologies amplifier using TaqMan Validated SNP Genotyping Assay kits (Applied Biosystems). The results were analyzed using Chi-square and the Fisher’s exact tests. Results: We found an association of GRIN2A rs7206256 and rs11644461 and GRIN2B rs7313149 with the early onset (before the age of 18 years old) schizophrenia. We did not reveal any associations of GRIN2A and GRIN2B polymorphisms with leading (positive vs. negative) symptoms or type of course (continuous vs. episodic) of schizophrenia. Conclusions: In the study, we confirmed the involvement of the GRIN2A and GRIN2B genes in the early onset of schizophrenia in a Russian population of the Siberian region

Comparative Characteristics of the Metabolic Syndrome Prevalence in Patients With Schizophrenia in Three Western Siberia Psychiatric Hospitals

Objective: The purpose of this study was to compare the prevalence of MetS and the associated sociodemographic, clinical, and pharmacotherapeutic characteristics of patients with schizophrenia in three psychiatric hospitals in the West Siberian region. Methods: Patients with a clinical diagnosis of schizophrenia (ICD-10: F20) and an age between 18 and 60 years were included in the study after giving informed consent. Metabolic syndrome was diagnosed according to the International Diabetes Federation criteria. This research was carried out at three Western Siberian psychiatric hospitals in Kemerovo, Tomsk, and Omsk. The study population included respectively 94, 131, and 91 inpatients with schizophrenia. We carried out schizophrenia symptoms assessment by PANSS, antipsychotic therapy evaluation, anthropometry, and biochemical analysis. Statistical Analysis included the Shapiro–Wilk test, non-parametric Kruskal–Wallis H-test for independent samples, Mann–Whitney U-test for independent samples, the chi-square test, stepwise multiple regression analyses. The level of significance was p < 0.05. Results: The metabolic syndrome prevalence was higher among patients in Tomsk (36.6%), compared with Kemerovo (20.2%, p = 0.008) or Omsk (18.7%, p = 0.004), mainly due to the high prevalence of abdominal obesity, while men from Tomsk were more susceptible to this condition than men from other regions (p < 0.05). Patients from Omsk had the highest severity schizophrenia symptoms according to PANSS, and patients from Tomsk had the lowest severity of positive symptoms according to PANSS. Patients from Tomsk had the minimum duration of antipsychotic therapy compared with the patient from Kemerovo (p = 0.017) and from Omsk (p = 0.000019), but most patients from Tomsk received second-generation atypical antipsychotics, while patients from Omsk received mainly conventional antipsychotics (p = 0.0001). Multiple regression analysis showed that metabolic syndrome associated with schizophrenia duration and body mass index, although the association was not so strong (adjusted R(2) = 0.2435, p < 0.0001). Discussion: The study illustrates that in different psychiatric hospitals within the same region, the prevalence of metabolic syndrome in patients with schizophrenia can vary significantly, which dictates the need to look for opportunities to minimize the risk of its occurrence, taking into account the experience of each hospital

EMBRIOGENESIS OF NEURONAL ELENENTS (GLIOBLASTS AND GABAA RECEPTORS) IN THE HUMAN BRAIN NEUROIMMUNE SYSTEM UNDER PRENATAL ALCOHOL EXPOSURE

Exposure to alcohol causes imbalances in neuroimmune function and impaired brain development. Alcohol activates the innate immune signaling pathways in the brain. Neuroimmune molecules expressed and secreted by glial cells of the brain (microglia, oligodendroglia) alter the function of neurons and further stimulate the development of alcoholic behavior. Various signaling pathways and brain cells are involved in the transmission of neuroimmune signals. Glial cells are the main sources of immune mediators in the brain, which respond to and release immune signals in the central nervous system. The aim of this study was to study neuronal elements: morphometric parameters of glioblasts, synaptic structures and properties of synaptosomal GABAA-benzodiazepine receptors of the neuroimmune system in the embryogenesis of the human brain under perinatal exposure to alcohol. Changes in glioblasts in the brain tissue of human embryos and fetuses were revealed under conditions of chronic prenatal alcoholization with an increase in gestational age compared with control subgroups: a significant increase in the average number of glioblasts, the length of the perimeters of presynaptic terminal structures, postsynaptic density, presynaptic terminal regions were significantly less (p &lt; 0.01) in the study group than in the control comparison group. Exposure to ethanol leads to a decrease in the affinity of GABAA-benzodiazepine receptors, which affects neuronal plasticity associated with the development and differentiation of progenitor cells (glioblasts and neuroblasts) during embryogenesis of the human brain and leads to suppression of GABAergic function in the brain. This causes a disruption in the interconnection of embryonic cells in the brain, leads to excessive apoptosis due to the activation of glial cells of the nervous tissue, disruption of neuroimmune function in the developing brain, changes in neuronal circuits, as well as a change in the balance of excitatory and inhibitory effects, which affects the functional activity in the central nervous system. Glial activation is a compensatory reaction caused by neuroplastic changes aimed at adapting the developing brain of the embryo and fetus under conditions of neurotoxicity and hypoxia under the influence of prenatal alcoholization of the maternal organism and the effect of ethanol on the fetus. The dynamics of changes in glial elements and receptor activity in the nervous tissue of human embryos and fetuses under conditions of prenatal exposure to alcohol indicates a more pronounced effect of alcohol on the earliest stages of human embryo development, which is of great practical importance in planning pregnancy and the inadmissibility of alcoholization of the mother in order to avoid negative consequences in offspring

Climate Change, Growth, and California Wildfire

Large wildfire occurrence and burned area are modeled using hydroclimate and landsurface characteristics under a range of future climate and development scenarios. The range of uncertainty for future wildfire regimes is analyzed over two emissions pathways (the Special Report on Emissions Scenarios [SRES] A2 and B1 scenarios); three global climate models (Centre National de Recherches Météorologiques CM3, Geophysical Fluid Dynamics Laboratory CM21 and National Center for Atmospheric Research PCM2); a mid‐range scenario for future population growth and development footprint; two model specifications related to the uncertainty over the speed and timing with which vegetation characteristics will shift their spatial distributions in response to trends in climate and disturbance; and two thresholds for defining the wildland‐urban interface relative to housing density. Results were assessed for three 30‐year time periods centered on 2020, 2050, and 2085, relative to a 30‐year reference period centered on 1975. Substantial increases in wildfire are anticipated for most scenarios, although the range of outcomes is large and increases with time. The increase in wildfire area burned associated with the higher emissions pathway (SRES A2) is substantial, with increases statewide ranging from 57 percent to 169 percent by 2085, and increases exceeding 100 percent in most of the forest areas of Northern California in every SRES A2 scenario by 2085. The spatial patterns associated with increased fire occurrence vary according to the speed with which the distribution of vegetation types shifts on the landscape in response to climate and disturbance, with greater increases in fire area burned tending to occur in coastal southern California, the Monterey Bay area and northern California Coast ranges in scenarios where vegetation types shift more rapidly.National Oceanic and Atmospheric Administration (NOAA) Regional Integrated Science and Assessment Program for California, United StatesCalifornia Climate Change Center/[CEC-500-2009-046-F]//Estados UnidosUnited States Department of Agriculture (USDA) Forest Service Pacific Southwest Research Station///Estados UnidosNational Oceanic and Atmospheric Administration (NOAA) Regional Integrated Science and Assessment Program for California///Estados UnidosUCR::Vicerrectoría de Investigación::Unidades de Investigación::Ciencias Básicas::Centro de Investigaciones Geofísicas (CIGEFI