Central Nervous System Structures Research Articles

Unraveling the Intricacies of OPG/RANKL/RANK Biology and Its Implications in Neurological Disorders-A Comprehensive Literature Review.

The OPG/RANKL/RANK framework, along with its specific receptors, plays a crucial role in bone remodeling and the functioning of the central nervous system (CNS) and associated disorders. Recent research and investigations provide evidence that the components of osteoprotegerin (OPG), receptor activator of NF-kB ligand (RANKL), and receptor activator of NF-kB (RANK) are expressed in the CNS. The CNS structure encompasses cells involved in neuroinflammation, including local macrophages, inflammatory cells, and microglia that cross the blood-brain barrier. The OPG/RANKL/RANK trio modulates the neuroinflammatory response based on the molecular context. The levels of OPG/RANKL/RANK components can serve as biomarkers in the blood and cerebrospinal fluid. They act as neuroprotectants following brain injuries and also participate in the regulation of body weight, internal body temperature, brain ischemia, autoimmune encephalopathy, and energy metabolism. Although the OPG/RANKL/RANK system is primarily known for its role in bone remodeling, further exploring deeper into its multifunctional nature can uncover new functions and novel drug targets for diseases not previously associated with OPG/RANKL/RANK signaling.

Эффекты воздействий радиочастотных электромагнитных полей на нервную систему. Эксперименты in vitro (обзор)

The effects of mobile communications on the population, primarily on children and adolescents as the cohort most vulnerable to any environmental factors, dictates the need for a thorough investigation into the impact of radio frequency electromagnetic fields (RF EMF) on the central nervous system (CNS) as the main target of their action. In this regard, the analysis of experimental data as an indirect assessment of possible negative changes in the body of young animals under the influence of RF EMF, including 5G and Wi-Fi, is highly relevant. We performed a systematization of experimental data, which will be presented in two parts: in vitro and in vivo experiments. This article introduces materials indicating both diversity of approaches to studying the effects of RF EMF on the central nervous system and difficulties of systematizing the results of the experiments. The analysis of literature data showed that, despite the numerous studies into the effects of RF EMF in vitro, CNS cell cultures are used rather rarely. However, this paper examines in detail the results of in vitro experiments: changes in the action potential, morphological changes in cells and the myelin sheath, and changes in the permeability of the blood–brain barrier (using cultures of only nerve cells). It was established that, despite some inconsistency in the results obtained, most studies indicate a negative effect of RF EMF on CNS cells. The morphological and histological changes in CNS structures under the influence of RF EMF will be presented in the next part of the review.

ВЛИЯНИЕ ИНФОРМАЦИОННОГО СТРЕССА НА ПСИХИЧЕСКОЕ ЗДОРОВЬЕ НАСЕЛЕНИЯ

The abundance of diverse information accompanied by information noise can be an additional and powerful stressor, especially if the assimilation and processing of this information is carried out in a time-limited environment. Information streams created by gadgets, reflecting the activity of a person in social networks, his communications, his news sources, are not a harmless source of leisure and recreation. They require the inclusion of sensory systems and central nervous system structures, which are very energy-intensive. Manifestations of information fatigue are clinically similar to stress symptoms, and have common neurobiological mechanisms based on adaptation to changes or new challenges. The emergence of new phenomena of interaction with information space and technogenic environment (FOMO) reflects the influence of information transmitted by gadgets on the mental health of the population. Cognitive flexibility, goal-setting, will-based control, priority-setting, and gadget-detox (gadget regulation and informed information consumption) are all necessary skills for successful interaction with and operation of information flows.

Increased levels of advanced oxidation protein products (AOPPs) were associated with nociceptive behavior and clinical scores in an experimental progressive autoimmune encephalomyelitis model (PMS-EAE).

Multiple sclerosis (MS) is a neurodegenerative disease that affects the central nervous system (CNS) generating neuropathic pain and anxiety. Primary progressive MS (PPMS) is the most disabling clinical form, and the patients present an intense neurodegenerative process. In this context, the advanced oxidation protein products (AOPPs) are oxidized compounds and their accumulation in plasma has been related to clinical disability in MS patients. However, the involvement of AOPPs in neuropathic pain- and anxiety-like symptoms was not previously evaluated. To assess this, female mice C57BL/6J were used to induce progressive experimental autoimmune encephalomyelitis (PMS-EAE). Clinical score, weight, strength of plantar pressure, rotarod test, mechanical allodynia, and cold hypersensitivity were evaluated before induction (baseline) and on days 7th , 10th , and 14th post-immunization. We assessed nest building, open field, and elevated plus-maze tests 13 days post-immunization. Animals were killed at 14 days post-immunization; then, AOPPs levels, NADPH oxidase, and myeloperoxidase (MPO) activity were measured in the prefrontal cortex, hippocampus, and spinal cord samples. The clinical score increased 14th post-immunization without changes in weight and mobility. Reduced paw strength, mechanical allodynia, and cold allodynia increased in the PMS-EAE animals. PMS-EAE mice showed spontaneous nociception and anxiety-like behavior. AOPPs concentration, NADPH oxidase, and MPO activity increase in CNS structures. Multivariate analyses indicated that the rise of AOPPs levels, NADPH oxidase, and MPO activity influenced the clinical score and cold allodynia. Thus, we indicated the association between non-stimuli painful perception, anxiety-like, and CNS oxidative damage in the PMS-EAE model.

Delivery of Adeno-Associated Virus Vectors to the Central Nervous System for Correction of Single Gene Disorders.

Genetic disorders of the central nervous system (CNS) comprise a significant portion of disability in both children and adults. Several preclinical animal models have shown effective adeno-associated virus (AAV) mediated gene transfer for either treatment or prevention of autosomal recessive genetic disorders. Owing to the intricacy of the human CNS and the blood-brain barrier, it is difficult to deliver genes, particularly since the expression of any given gene may be required in a particular CNS structure or cell type at a specific time during development. In this review, we analyzed delivery methods for AAV-mediated gene therapy in past and current clinical trials. The delivery routes analyzed were direct intraparenchymal (IP), intracerebroventricular (ICV), intra-cisterna magna (CM), lumbar intrathecal (IT), and intravenous (IV). The results demonstrated that the dose used in these routes varies dramatically. The average total doses used were calculated and were 1.03 × 1013 for IP, 5.00 × 1013 for ICV, 1.26 × 1014 for CM, and 3.14 × 1014 for IT delivery. The dose for IV delivery varies by patient weight and is 1.13 × 1015 IV for a 10 kg infant. Ultimately, the choice of intervention must weigh the risk of an invasive surgical procedure to the toxicity and immune response associated with a high dose vector.

Humanized brain organoids-on-chip integrated with sensors for screening neuronal activity and neurotoxicity.

The complex structure and function of the human central nervous system that develops from the neural tube made in vitro modeling quite challenging until the discovery of brain organoids. Human-induced pluripotent stem cells-derived brain organoids offer recapitulation of the features of early human neurodevelopment in vitro, including the generation, proliferation, and differentiation into mature neurons and micro-macroglial cells, as well as the complex interactions among these diverse cell types of the developing brain. Recent advancements in brain organoids, microfluidic systems, real-time sensing technologies, and their cutting-edge integrated use provide excellent models and tools for emulation of fundamental neurodevelopmental processes, the pathology of neurological disorders, personalized transplantation therapy, and high-throughput neurotoxicity testing by bridging the gap between two-dimensional models and the complex three-dimensional environment in vivo. In this review, we summarize how bioengineering approaches are applied to mitigate the limitations of brain organoids for biomedical and clinical research. We further provide an extensive overview and future perspectives of the humanized brain organoids-on-chip platforms with integrated sensors toward brain organoid intelligence and biocomputing studies. Such approaches might pave the way for increasing approvable clinical applications by solving their current limitations.

Comprehensive Analysis of the Spatial Distribution of Gadolinium, Iron, Manganese, and Phosphorus in the Brain of Healthy Rats After High-Dose Administrations of Gadodiamide and Gadobutrol.

After the administration of gadolinium-based contrast agents (GBCAs), residual gadolinium (Gd) has been detected in a few distinct morphological structures of the central nervous system (CNS). However, a systematic, comprehensive, and quantitative analysis of the spatial Gd distribution in the entire brain is not yet available. The first aim of this study is to provide this analysis in healthy rats after administration of high GBCA doses. The second aim is to assess the spatial distributions and possible Gd colocalizations of endogenous iron (Fe), manganese (Mn), and phosphorus (P). In addition, the presence of Gd in proximity to blood vessels was assessed by immunohistochemistry. Male rats were randomly assigned to 3 groups (n = 3/group): saline (control), gadodiamide (linear GBCA), and gadobutrol (macrocyclic GBCA) with cumulative Gd doses of 14.4 mmol/kg of body mass. Five weeks after the last administration, the brains were collected and cryosectioned. The spatial distributions of Gd, Fe, Mn, and P were analyzed in a total of 130 sections, each covering the brain in 1 of the 3 perpendicular anatomical orientations, using laser ablation coupled with inductively coupled plasma mass spectrometry. Quantitative spatial element maps were generated, and the concentrations of Gd, Fe, and Mn were measured in 31 regions of interest covering various distinct CNS structures. Correlation analyses were performed to test for possible colocalization of Gd, Fe, and Mn. The spatial proximity of Gd and blood vessels was studied using metal-tagged antibodies against von Willebrand factor with laser ablation coupled with inductively coupled plasma mass spectrometry. After administration of linear gadodiamide, high Gd concentrations were measured in many distinct structures of the gray matter. This involved structures previously reported to retain Gd after linear GBCA, such as the deep cerebellar nuclei or the globus pallidus, but also structures that had not been reported so far including the dorsal subiculum, the retrosplenial cortex, the superior olivary complex, and the inferior colliculus. The analysis in all 3 orientations allowed the localization of Gd in specific subregions and layers of certain structures, such as the hippocampus and the primary somatosensory cortex. After macrocyclic gadobutrol, the Gd tissue concentration was significantly lower than after gadodiamide. Correlation analyses of region of interest concentrations of Gd, Fe, and Mn revealed no significant colocalization of Gd with endogenous Fe or Mn in rats exposed to either GBCA. Immunohistochemistry revealed a colocalization of Gd traces with vascular endothelium in the deep cerebellar nuclei after gadobutrol, whereas the majority of Gd was found outside the vasculature after gadodiamide. In rats exposed to gadodiamide but not in rats exposed to gadobutrol, high Gd concentrations were measured in various distinct CNS structures, and structures not previously reported were identified to contain Gd, including specific subregions and layers with different cytoarchitecture and function. Knowledge of these distinct spatial patterns may pave the way for tailored functional neurological testing. Signs for the localization of the remaining Gd in the vascular endothelium were prominent for gadobutrol but not gadodiamide. The results also indicate that local transmetalation with endogenous Fe or Mn is unlikely to explain the spatial patterns of Gd deposition in the brain, which argues against a general role of these metals in local transmetalation and release of Gd ions in the CNS.

Expansion modes of primate nervous system structures in the light of the Prosomeric Model

The expansion of human and non-human primate central nervous system structures has been a paramount question for classic and contemporary studies in comparative vertebrate neuroanatomy. These studies can benefit from framing data analysis within the Prosomeric Model, which defines a common Bauplan for all vertebrate species, including mammals. According to this model, the vertebrate nervous system is composed of several Fundamental Morphological Units (FMUs) that are defined and delineated by characteristic gene expression profiles. Thus, the expansion of neural structures can be traced back to heterochronic neurogenesis, cell lineage specification, and axon growth in their corresponding FMUs. In the present article, we exemplify the use of the Prosomeric Model as the proper theoretical framework for analyzing the expansion of the cerebral and cerebellar cortices, the pontine nuclei, the striatum, the nigrostriatal dopaminergic system, the thalamus, and the amygdala in primates compared to rodents. We describe the quantitative (volume and neuron number) and qualitative (cytoarchitectonic and cell type differences) expansion of these structures in primates versus rodents and define different expansion modes. Then, we relate these modes to the developmental primary events of specification and secondary events of histogenesis, like neurogenesis. We conclude that the systematic analysis of the molecular regulation of primary and secondary developmental events in each FMU in rats, primates, and other mammals could provide the necessary insight to identify the causal mechanisms of the expansion modes described in the present article.

Neurotoxicity of Glyphosate to Planarian Dugesia japonica.

As one of the most widely used herbicides in agricultural industry, the residues of glyphosate (GLY) are frequent environmental pollutants. Freshwater planarian Dugesia japonica has been developed as a model for neurotoxicology. In this study, the effects of GLY on locomotion and feeding behavior, as well as neuroenzyme activities and mRNA expressions of D. japonica were determined. Additionally, histochemical localization was executed to explore the damage to the central nervous system (CNS) of planarians stressed by GLY. The results showed that the locomotor velocity, ingestion rate and the neuroenzyme activity were inhibited and the gene expressions were altered. Also, histo-architecture injury to CNS of planarians upon GLY exposure in a time-dependent manner was observed. Collectively, our results indicate that GLY can cause neurotoxicity to freshwater planarians representing as reduction in locomotor velocity and feeding rate by disturbing the neurotransmission systems and damaging the structure of CNS.

Exploring the significance of lipids in Alzheimer's disease and the potential of extracellular vesicles.

Lipids play a significant role in maintaining central nervous system (CNS) structure and function, and the dysregulation of lipid metabolism is known to occur in many neurological disorders, including Alzheimer's disease. Here we review what is currently known about lipid dyshomeostasis in Alzheimer's disease. We propose that small extracellular vesicle (sEV) lipids may provide insight into the pathophysiology and progression of Alzheimer's disease. This stems from the recognition that sEV likely contributes to disease pathogenesis, but also an understanding that sEV can serve as a source of potential biomarkers. While the protein and RNA content of sEV in the CNS diseases have been studied extensively, our understanding of the lipidome of sEV in the CNS is still in its infancy.

Neural tube defects: current view on etiology, prenatal prevention, and early diagnosis. A review

A literature review on the etiology, prevention, and early diagnosis of neural tube defects is presented, focusing on the causes and risk factors for these disorders. Various pathogenetic mechanisms for neural tube defects and the role of folic acid in their prevention are described. The main stages of ultrasound evaluation of the central nervous system structures in the first trimester of pregnancy are addressed. A basic ultrasound imaging technique that allows to identify spina bifida is provided. This review aims to present current data on the etiology, prevention, and early diagnosis of neural tube defects. A search was conducted in domestic and foreign literature databases (eLIBRARY, Medline/PubMed, Embase, Crossref, RSCI) using the keywords "neural tube defect," "spina bifida," "prenatal diagnosis," "folic acid," "meningomyelocele," "myeloschisis." Twenty-five papers met the selection criteria and were included in the review. Healthcare providers' awareness of the methods of prenatal prophylaxis and the possibilities of early perinatal ultrasound diagnosis of neural tube defects will reduce their incidence and infant morbidity rates and increase the effectiveness of medical care.

Effect of Subliminal Auditory Stimulation on Components of Auditory Late Responses and Functional Magnetic Resonance Imaging Data in Adults with Normal Hearing

Background and Aim: The use of subliminal stimulation for unconscious effects on the target population is of great importance. while several studies have generated proper visual and auditory stimuli for subliminal stimulation, no study was found on the long-term effects of it. Therefore, this study aims to investigate the long-term effects of auditory subliminal presentation on the central nervous system structures using fMRI and Auditory Late Responses (ALRs).
 Methods: Participants were 26 students with a mean age of 24.03±2.32 years. There was four group in study. First, fMRI was done and ALRs were recorded for all of them. Then, music files containing words embedded in them was presented subliminally to participants in groups A and B for 10 days, group C received music file without any subliminal stimuli and group D was control group. It was repeated after 10 days.
 Results: The subliminal stimuli had significant effects on the amplitudes of P1, N1, P2, and P3 waves (F3=25.03, 25.41, 39.11, and 14.60; p<0.001). Between-group comparison showed significant changes in groups A and B compared to groups C and D (p<0.05). The difference in the recorded potential mean values showed the highest change for recording electrodes in the prefrontal, frontal, and central regions and the lowest change in parietal and occipital regions. There was no significant change for a latency component.
 Conclusion: Subliminal stimuli, presented appropriately and continuously, can leave long- term effects on the central nervous system structure causing extensive changes in the people’s attitude to a certain subject.
 Keywords: Subliminal perception; unconscious perception; unconsciousness; subconsciousness; subliminal auditory stimulus

Yap controls notochord formation and neural tube patterning by integrating mechanotransduction with FoxA2 and Shh expression.

Correct notochord and neural tube (NT) formation is crucial to the development of the central nervous system and midline structures. Integrated biochemical and biophysical signaling controls embryonic growth and patterning; however, the underlying mechanisms remain poorly understood. Here, we took the opportunities of marked morphological changes during notochord and NT formation and identified both necessary and sufficient roles of Yap, a key mechanosensor and mechanotransducer, in biochemical signaling activation during formation of notochord and floor plate, the ventral signaling centers that pattern the dorsal-ventral axis of NT and the surrounding tissues. We showed that Yap activation by a gradient of mechanical stress and tissue stiffness in the notochord and ventral NT induces FoxA2 and Shh expression. Hedgehog signaling activation rescued NT patterning defects caused by Yap deficiency, but not notochord formation. Therefore, mechanotransduction via Yap activation acts in feedforward mechanisms to induce FoxA2 expression for notochord formation and activate Shh expression for floor plate induction by synergistically interacting with FoxA2.

Neuron-astrocyte omnidirectional signaling in neurological health and disease.

Astrocytes are an abundantly distributed population of glial cells in the central nervous system (CNS) that perform myriad functions in the normal and injured/diseased brain. Astrocytes exhibit heterogeneous phenotypes in response to various insults, a process known as astrocyte reactivity. The accuracy and precision of brain signaling are primarily based on interactions involving neurons, astrocytes, oligodendrocytes, microglia, pericytes, and dendritic cells within the CNS. Astrocytes have emerged as a critical entity within the brain because of their unique role in recycling neurotransmitters, actively modulating the ionic environment, regulating cholesterol and sphingolipid metabolism, and influencing cellular crosstalk in diverse neural injury conditions and neurodegenerative disorders. However, little is known about how an astrocyte functions in synapse formation, axon specification, neuroplasticity, neural homeostasis, neural network activity following dynamic surveillance, and CNS structure in neurological diseases. Interestingly, the tripartite synapse hypothesis came to light to fill some knowledge gaps that constitute an interaction of a subpopulation of astrocytes, neurons, and synapses. This review highlights astrocytes' role in health and neurological/neurodegenerative diseases arising from the omnidirectional signaling between astrocytes and neurons at the tripartite synapse. The review also recapitulates the disruption of the tripartite synapse with a focus on perturbations of the homeostatic astrocytic function as a key driver to modulate the molecular and physiological processes toward neurodegenerative diseases.

The introduction and current status of the multidimensional model of pain neurobiology.

Conceptual models are useful because they guide our practical actions related to whatever is represented by the model; this includes research that reveals the limitations of these actions and the potential for their improvement. These statements apply to many aspects of daily life and especially to pain as a challenge for both clinical practice specifically and neurobiology generally. In the first half of the 20th century, our conceptual model of pain, to the extent that it existed at all, was based on evidence supporting the proposition that pain emerged from activity within a very spatially limited set of central nervous system (CNS) structures located within the cerebral cortex and it's oligosynaptic connections with the thalamus. This CNS activity was strongly associated with the activation of physiologically distinct and specialized somatovisceral afferent fibers. All, or nearly all, aspects of the pain experience were thought to arise from, and be modified by, changes in that localized CNS activity. There was no compelling and widely accepted reason to consider an alternative model. However, neurophysiological, neuroanatomical, behavioral, and clinical evidence emerging in the late mid-20th century prompted a reconsideration of the prevailing model of pain neurobiology. Based on this new evidence and the perceived limitations of the prevailing model, pain could then be reasonably conceived as a multidimensional experience arising from the conjoint activation of physiologically and anatomically distinct but interacting CNS structures each separately mediating sensory discriminative, affective, and cognitive aspects of pain. This brief historical review describes the intellectual climate at the time this multidimensional model was proposed, the dispositions for resisting or accepting it, and concludes with a comment on the current status of the model as a fusion of distributed activations that create a unified perception of pain.

A Rare Case Report of a Vertebral Artery Variant Arising From the Aorta With Its Clinical Significance: An Uncommon Anatomy Unveiled

The vertebrobasilar (VB) system, comprising two vertebral arteries and one basilar artery, is responsible for providing vital vascular supply to the central nervous system structures. Disruption in this network can lead to fatal neurologic outcomes, and variations in the origin of vessels may contribute to unexplained symptoms of clinical relevance. Therefore, an extensive understanding of the VB system's anatomy and its variations is crucial for diagnosing neurological disorders. Here, we report a case of a vertebral artery variant arising from the aortic arch proximal to the left subclavian artery in the cadaver of a 50-year-old male, discovered incidentally during a teaching dissection session. We also discuss the clinical pathophysiology and the relevance of the neurological symptoms in relation to the anomaly.

BMPRII+ neural precursor cells isolated and characterized from organotypic neurospheres: an in vitro model of human fetal spinal cord development.

Roof plate secretion of bone morphogenetic proteins (BMPs) directs the cellular fate of sensory neurons during spinal cord development, including the formation of the ascending sensory columns, though their biology is not well understood. Type-II BMP receptor (BMPRII), the cognate receptor, is expressed by neural precursor cells during embryogenesis; however, an in vitro method of enriching BMPRII+ human neural precursor cells (hNPCs) from the fetal spinal cord is absent. Immunofluorescence was undertaken on intact second-trimester human fetal spinal cord using antibodies to BMPRII and leukemia inhibitory factor (LIF). Regions of highest BMPRII+ immunofluorescence localized to sensory columns. Parenchymal and meningeal-associated BMPRII+ vascular cells were identified in both intact fetal spinal cord and cortex by co-positivity with vascular lineage markers, CD34/CD39. LIF immunostaining identified a population of somas concentrated in dorsal and ventral horn interneurons, mirroring the expression of LIF receptor/CD118. A combination of LIF supplementation and high-density culture maintained culture growth beyond 10 passages, while synergistically increasing the proportion of neurospheres with a stratified, cytoarchitecture. These neurospheres were characterized by BMPRII+/MAP2ab+/-/βIII-tubulin+/nestin-/vimentin-/GFAP-/NeuN- surface hNPCs surrounding a heterogeneous core of βIII-tubulin+/nestin+/vimentin+/GFAP+/MAP2ab-/NeuN- multipotent precursors. Dissociated cultures from tripotential neurospheres contained neuronal (βIII-tubulin+), astrocytic (GFAP+), and oligodendrocytic (O4+) lineage cells. Fluorescence-activated cell sorting-sorted BMPRII+ hNPCs were MAP2ab+/-/βIII-tubulin+/GFAP-/O4- in culture. This is the first isolation of BMPRII+ hNPCs identified and characterized in human fetal spinal cords. Our data show that LIF combines synergistically with high-density reaggregate cultures to support the organotypic reorganization of neurospheres, characterized by surface BMPRII+ hNPCs. Our study has provided a new methodology for an in vitro model capable of amplifying human fetal spinal cord cell numbers for > 10 passages. Investigations of the role BMPRII plays in spinal cord development have primarily relied upon mouse and rat models, with interpolations to human development being derived through inference. Because of significant species differences between murine biology and human, including anatomical dissimilarities in central nervous system (CNS) structure, the findings made in murine models cannot be presumed to apply to human spinal cord development. For these reasons, our human in vitro model offers a novel tool to better understand neurodevelopmental pathways, including BMP signaling, as well as spinal cord injury research and testing drug therapies.

Administration of prosaposin-derived neurotrophic factor to neural tube defects facilitates regeneration and restores neurological functions.

Neural tube defects (NTDs) cause fetal and pediatric deaths or lifelong neurological disabilities. No effective treatment is currently available for NTDs. We attempted to elucidate the pathogenesis of NTDs and propose a therapeutic strategy. Intra-amniotic treatment with prosaposin-derived 18-mer peptide (PS18) protected the spinal cord from secondary damage and rescued neurological function in an established chicken model of spina bifida aperta (SBA), the severe type of NTDs. PS18 promoted the formation of a neuroectodermal covering over the defective neural tube within 24-h after treatment, enhanced the regeneration/restoration process, and decreased apoptotic activity in the developing spinal cord. PS18 reduced the SBA wound and almost completely formed the spinal cord. SBA chicks that received PS18 exhibited relatively normal walking and sensorimotor responses, and reduced pain-associated behavior in postnatal life. In conclusion, PS18 is a promising therapeutic agent for NTDs and may be useful for treating other types of spinal cord injuries.

The Association of the Hypothalamic-Pituitary-Adrenal Axis with Appetite Regulation in Children with Fetal Alcohol Spectrum Disorders (FASDs)

Prenatal alcohol exposure causes growth impairment and a wide range of developmental, physical, and cognitive disorders in children, collectively referred to as fetal alcohol spectrum disorders (FASDs). In the course of FASDs, abnormalities can also affect eating behavior and nutritional status, but these problems have received little attention. Therefore, the aim of our study was to determine the levels of hormones involved in the action of the hypothalamic-pituitary-adrenal axis: proopiomelanocortin (POMC), cortisol, and adrenocorticotropic hormone (ACTH), in the serum of patients with FASDs. To our knowledge, none of these hormones studied have yet been evaluated in FASDs to date. We investigated 62 FASD patients and 23 healthy controls by applying an enzyme-linked immunosorbent method (ELISA). Fasting POMC levels were significantly lower in patients with FASDs (10.97 vs. 18,57 ng/mL, p = 0.039) compared to controls. However, there were no differences in cortisol concentrations. Additionally, the sex and subgroup status (fetal alcohol syndrome (FAS), neurobehavioral disorder associated with prenatal alcohol exposure (ND-PAE), and FASD risk) did not affect hormone levels. POMC was positively correlated with some clinical parameters such as age, BMI percentile, carbohydrate biomarkers, and ACTH. A positive correlation was observed between ACTH and cortisol levels, as well as ACTH and cholesterol levels. Data analysis showed no HPA axis abnormalities in the form of elevated serum cortisol and ACTH levels. Differences in POMC concentration may indicate the involvement and/or impairment of central nervous system structures in hormonal alterations in FASD individuals, caused by prenatal alcohol exposure. Hormonal dysregulation in FASDs can contribute to reduced growth and development, as well as many other disturbed processes, including neurological/neurodevelopmental dysfunctions. Further insightful studies involving a larger group of patients are needed to determine the potential impact of the measured hormones.

The role of interleukin 10 in the development of the schizophrenia deficit syndrome in the light of the disconnection hypothesis

IntroductionOne of the subtypes of schizophrenia is the deficit syndrome (DS). Because of different risk factors, course, response to treatment weak prognosis, researches on this group of patients are important. Etiology of schizophrenia is often hypothesized as the inflammation process. Due to the imbalance of certain cytokines (interleukin-10 (IL-10) -antyinflamation cytokine, among others) changes in the function and structure of central nervous system may occur. That process could stand behind the outbreak of psychotic and deficit symptoms of the illness. Subinflammation can have an impact on the white matter structure. Disturbances in this area can cause impairment of cortical communication and hence, produce psychopathology. One of the structures that seem to have the basis of the deficit syndrome isinferior longitudinal fasciculus (ILF). ILF is a bundle of association fibers with interconnects temporal cortex with ocapital cortex.ObjectivesThe aim of our study was to investigate a relationship between the integrity of ILF and interleukin – 10.Methods39 schizophrenia subjects divided into two groups DS (16) and non-deficyt sydrome (NDS) (23) and 18 healthy controls (HC) participated in the study. A DTI analysis was performed on all study participants. The psychopathology of schizofrenia was assessed using the Positive and Negative Syndrome Scale (PANSS). The ILF analysis was then conducted using fractional anisotropy (FA) and mean diffusivity (MD) parameters. Blood samples were obtained to analyze serum level of IL-10 level.ResultsThe differences in FA value in left ILF between DS and HC group were confirmed. The difference in values of IL-10 between groups were not confirmed. A negative correlation was found between FA values in left ILF and IL-10 (p = 0.033) among DS group.ConclusionsThe imparment of the structure of ILF may be involved in ethiopatogenesis of DS. Moreover, changes in IL-10 levels may be related to the microstructure of ILF bundle.Disclosure of InterestNone Declared