Neuroendocrine Factors Research Articles

Cancer risk in polycystic ovary syndrome patients: Common treatments and future perspectives

In women of childbearing age, polycystic ovarian syndrome (PCOS) is the most common endocrine and metabolic condition. Ovulatory dysfunction, clinical symptoms of hyperandrogenism, and multiple cystic ovaries are the hallmarks of PCOS. Women who have PCOS may have irregular insulin activity in addition to other difficulties such as pattern hair loss, acne, obesity, infertility, and hirsutism. An unhealthy lifestyle, hereditary causes, androgen exposures, and neuroendocrine factors are frequently the causes of PCOS. This results in an unbalanced hormonal state, hyperandrogenism, high insulin, and inflammation. Due to the overlapping metabolic and endocrine issues, PCOS patients' cancer risk has been the subject of debate for decades.This review article examines the relationship between PCOS and various types of reproductive cancers, focusing on the possible reasons for cancer in PCOS patients.

Thymus mast cells as a component of neuro-endocrine-immune interactions under stress

Mast cells (MCs) are a required component of the thymus microenvironment. They affect intercellular interactions and permeability of the hematothymic barrier through cytokine production. There is speculation that the thymus is the site of MCs formation and deposition. MCs are under complex neuro-endocrine control and they can play an important role in the process of acute transformation of the thymus in the formation of a stress reaction, affecting the extrathymic migration of cells. The purpose of this study is to assess the functional involvement of MCs in the process of the thymus acute transformation at various hyper- and hypodynamic effects during the formation of stress response and without it.The study was conducted on male Wistar rats. The stress factors were physical activity (swimming) of different intensities and immobilization, which represent two opposite states of dynamic stress. MCs were classified on histological preparations; a degranulation coefficient and a mean histochemical coefficient (synthetic activity) were calculated.In groups with preserved adrenal glands after exposure a significant decrease in the thymus mass coefficient is noted, which indicates a weakening of its functional activity in response to the development of stress. At the same time, MCs of the thymus quickly respond to neuro-endocrine factors under stress. These cells are involved in a general reaction: their activity consists in a synchronous decrease of the synthesis of granules in the cytoplasm and an increased release of active substances accumulated earlier. The mass and structure of the thymus remain unchanged in groups with removed adrenal glands after immobilization. No changes in morphofunctional indicators of mast cells were detected either. Experiments with hypo- and hyperdinamic loading of animals with preserved and removed adrenal glands indicate that the MCs response is largely determined by the hypothalamic-pituitary-adrenal axis of the endocrine system. Removal of the adrenal glands (inability to release glucocorticoids) leads to a lack of functional response from the thymus MCs. The stimulating effect of adrenal glucocorticoids on MCs under stress is carried out in combination with other neuro-endocrine factors (catecholamines, corticotropin-releasing hormone, adrenocorticotropic hormone). When this axis is activated and a full-fledged stress reaction is formed by the body, MCs are actively involved in the process of acute transformation of the thymus through cytokine secretion. These is an important condition for the development of adaptation mechanisms by the immune system.

Polycystic ovary syndrome: Causes, symptoms, pathophysiology, and remedies

Polycystic ovary syndrome (PCOS), an endocrine and metabolic disorder during the reproductive age of women, is characterized by high androgen levels, irregular menses, and small cysts in the ovaries. One in 10 women worldwide is affected by PCOS. Women with PCOS might experience abnormal insulin activity, along with complications such as obesity, acne, pattern hair loss, mood swings, hirsutism, and infertility. PCOS is linked with severe clinical ailments such as type 2 diabetes (T2DM), cardiovascular diseases (CVDs), and cancer. The disease (PCOS) is often caused by a faulty lifestyle, neuroendocrine factors, genetic causes, and androgen exposures, leading to dysregulated hormonal state, hyperandrogenism, hyperinsulinemia, and inflammation. Society often preaches women to keep their physiological problems such as PCOS under the veil. Lack of conscience and the compulsion to abide by societal norms is often a barrier to the early diagnosis of PCOS. This review summarizes the causes, symptoms, pathophysiology, diagnosis, and possible treatment (medical, herbal, lifestyle improvement, acupuncture, and bariatric surgery) related to PCOS.

Influence of chronic stress on network states governing valence processing: Potential relevance to the risk for psychiatric illnesses.

Stress is a major risk factor for psychiatric illnesses and understanding the mechanisms through which stress disrupts behavioral states is imperative to understanding the underlying pathophysiology of mood disorders. Both chronic stress and early life stress alter valence processing, the process of assigning value to sensory inputs and experiences (positive or negative), which determines subsequent behavior and is essential for emotional processing and ultimately survival. Stress disrupts valence processing in both humans and preclinical models, favoring negative valence processing and impairing positive valence processing. Valence assignment involves neural computations performed in emotional processing hubs, including the amygdala, prefrontal cortex, and ventral hippocampus, which can be influenced by neuroendocrine mediators. Oscillations within and between these regions are critical for the neural computations necessary to perform valence processing functions. Major advances in the field have demonstrated a role for oscillatory states in valence processing under physiological conditions and emerging studies are exploring how these network states are altered under pathophysiological conditions and impacted by neuroendocrine factors. The current review highlights what is currently known regarding the impact of stress and the role of neuroendocrine mediators on network states and valence processing. Further, we propose a model in which chronic stress alters information routing through emotional processing hubs, resulting in a facilitation of negative valence processing and a suppression of positive valence processing.

Regulation of female sexual behavior and possibilities of drug therapy

Female sexual behavior is under the complex influence of psycho-emotional, neuroendocrine and social factors. The realization of normal sexual activity in women is possible if many conditions are met and, first of all, ensuring a positive psycho-emotional background, safety, a satisfactory state of health, as well as comfortable interpersonal relationships for most women. In addition to significant psychological and social impact, accumulated modern scientific data confirm the important role of neuro-hormonal regulation of sexual behavior and suggest the potential effectiveness of pharmacological therapy. Unfortunately, however, medical strategies for correcting female sexual disorders are limited. Currently, in some countries, several drugs that increase female sexual activity are allowed for use, however, all of them are not registered and are not approved for use on the territory of the Russian Federation. The article briefly describes the neural mechanisms of the main areas of the central nervous system underlying receptivity and sexual attraction, namely the olfactory and limbic systems, the neocortex. The main attention is paid to the function of neurotransmitters and hormones that are critically involved in the modulation of emotions and sexual behavior, including the inhibitory mediator of gamma aminobutyric acid (GABA), estrogens, testosterone, and the excitatory mediator glutamate. The stages of development, the results of experimental and clinical studies to assess the effectiveness and safety of the unique Russian neuropeptide drug Desirex, which is a stimulant of sexual behavior due to the mechanism of reversible suppression of the GABAergic system, nonspecific stimulation of the dopaminergic system of motivation and reinforcement of positive emotions and disinhibition of the controlling function of the neocortex, are presented in detail.

Exposure to Obesogenic Environments during Perinatal Development Modulates Offspring Energy Balance Pathways in Adipose Tissue and Liver of Rodent Models

Obesogenic environments such as Westernized diets, overnutrition, and exposure to glycation during gestation and lactation can alter peripheral neuroendocrine factors in offspring, predisposing for metabolic diseases in adulthood. Thus, we hypothesized that exposure to obesogenic environments during the perinatal period reprograms offspring energy balance mechanisms. Four rat obesogenic models were studied: maternal diet-induced obesity (DIO); early-life obesity induced by postnatal overfeeding; maternal glycation; and postnatal overfeeding combined with maternal glycation. Metabolic parameters, energy expenditure, and storage pathways in visceral adipose tissue (VAT) and the liver were analyzed. Maternal DIO increased VAT lipogenic [NPY receptor-1 (NPY1R), NPY receptor-2 (NPY2R), and ghrelin receptor], but also lipolytic/catabolic mechanisms [dopamine-1 receptor (D1R) and p-AMP-activated protein kinase (AMPK)] in male offspring, while reducing NPY1R in females. Postnatally overfed male animals only exhibited higher NPY2R levels in VAT, while females also presented NPY1R and NPY2R downregulation. Maternal glycation reduces VAT expandability by decreasing NPY2R in overfed animals. Regarding the liver, D1R was decreased in all obesogenic models, while overfeeding induced fat accumulation in both sexes and glycation the inflammatory infiltration. The VAT response to maternal DIO and overfeeding showed a sexual dysmorphism, and exposure to glycotoxins led to a thin-outside-fat-inside phenotype in overfeeding conditions and impaired energy balance, increasing the metabolic risk in adulthood.

Neurobiological Correlates Shared Between Obesity, BED and Food Addiction.

The ubiquity of the obesity condition in the United States, Europe and other regions with developed economies will associate to a significant adverse impact on public health. Numerous data indicate that social, behavioral, neuroendocrine, and metabolic factors may encourage compulsive eating behaviors thus increasing the risk of obesity. Several pathological conditions overlap with excess weight. Among the most common, there are binge eating disorder (BED) and food addiction (FA), which share several neurobiological and behavioral aspects with substance addictions. BED has many features in common with addictive behavior, such as loss of control and the need to frequently repeat the dysfunctional pattern despite negative consequences. The food addiction hypothesis assumes that exposure to highly palatable foods alters the reward circuits of the brain, resulting in a behavioral phenotype similar to substance addiction and facilitating dysfunctional eating behaviors, such as binge eating crises. In this review, over 100 publications, researched on MEDLINE from 2000 until march 2021, were included since they evaluate neuroendocrine changes, emotional homeostatic factors and the reward circuit, associating them with exposure to highly palatable foods, loss of control, the way we eat, the increase in impulsiveness and the inability to change eating behavior despite the negative consequences related to overweight and obesity. Finally, understanding the underlying neurobiological circuits of compulsive eating behaviors and food addiction could result in a great therapeutic potential for patients suffering from ailments nutrition and obesity.

State Anxiety and Procrastination: The Moderating Role of Neuroendocrine Factors.

Procrastination is prevalent among students, as well as the general population, and has negative impacts on various domains. Several models aimed to understand factors associated with procrastination, with some suggesting that anxiety plays a significant role. Biological factors have been shown to contribute to individual differences in procrastination; however, little attention has been paid to the role of neuroendocrine factors on procrastination. The primary question addressed in the present study is whether neuroendocrine factors (testosterone and cortisol) moderate the association between state anxiety and procrastination. Eighty-eight participants (29 men; 32 women using oral contraceptives; and 27 women not using oral contraceptives and in their luteal phase) were tested for biomarkers and completed questionnaires. Results show that state anxiety is positively correlated with procrastination. Furthermore, testosterone levels moderate the correlation between state anxiety and procrastination. As testosterone levels drop, the positive correlation between state anxiety and procrastination becomes stronger, but when testosterone levels are higher, no significant association between state anxiety and procrastination is found. Cortisol levels do not moderate the relationship between state anxiety and procrastination. The role of neuroendocrine factors for psychological outcomes is discussed.

Relationship of Depression, Anxiety, and Bipolar Disease with Burning Mouth Syndrome: A Nationwide Cohort Study.

Burning mouth syndrome (BMS) is a chronic, painful condition of the oral mucosa. Although the pathogenesis remains unclear, psychological and neuroendocrine factors are considered the major contributors. Few longitudinal studies have investigated the effects of psychological factors on the occurrence of BMS. Therefore, we evaluated the risk of BMS in patients with affective disorders using a nationwide population-based cohort dataset. We identified patients with depression, anxiety, and bipolar disorder and then selected comparison participants using the 1:4 propensity score-matching method. We investigated the incidence of BMS events during the follow-up period using survival analysis, the log-rank test, and Cox proportional hazards regression models. After adjusting for other contributing conditions, the adjusted hazard ratio (HR) for developing BMS was 3.37 (95% confidence interval [CI]: 1.67-6.80) for depression and 5.09 (95% CI: 2.19-11.80) for anxiety; however, bipolar disorder showed no significant risk. Specifically, female patients with depression and anxiety had an increased risk of BMS. Moreover, patients with anxiety showed an increased adjusted HR of BMS events during the first 4 years after diagnosis, whereas patients with depression did not. In conclusion, depression and anxiety disorders are significantly associated with the risk of BMS. Additionally, female patients showed a significantly higher risk of BMS than male patients, and anxiety showed increased BMS events earlier than depression. Therefore, clinicians should consider the risk of BMS when treating patients with depression or anxiety.

Association between non-high density lipoprotein-cholesterol fractions and presence of allostatic load among industrial workers

Objectives: Non-high density lipoprotein-cholesterol (non-HDL-C) fraction is the total cholesterol (TC) minus HDL-C. It is not a routinely reported component of lipid profile and is used in lipoprotein lowering therapy and prediction of coronary artery disease, target organ damage and atherosclerosis. Allostatic load (AL) is an imbalance between repetitive chronic exposure to stress and adaptive response. The present study investigates the association between non-HDL-C and its fractions (non-HDL-C/HDL-C, non-HDL-C/TC, non-HDL-C/ triglyceride [TG] and non-HDL-C/low-density lipoprotein-cholesterol [LDL-C]) and the presence of AL to determine, which fractions of non-HDL-C predict the diagnostic accuracy and optimal cut points. Materials and Methods: The study design is cross-sectional and data were collected from 169 male industrial workers. AL was measured using neuroendocrine (cortisol and dehydroepiandrosterone sulphate), cardiovascular (systolic blood pressure, diastolic blood pressure and heart rate), metabolic (TC, TG, HDL-C and LDL-C) and anthropometric (waist-hip ratio and body mass index) factors. The fractions of non-HDL-C/HDL-C, nonHDL-C/TC, non-HDL-C/TG and non-HDL-C/LDL-C were calculated using non-HDL-C, HDL-C, TC, TG and LDL-C values. Results: About 43.2% and 56.8% of workers had low and high AL, respectively. The non-HDL-C and its fractions such as non-HDL-C/HDL-C, non-HDL-C/TC and non-HDL-C/LDL-C were significantly increased in the high AL group. Stepwise regression analysis was used to examine the association between non-HDL-C fractions and AL. The fractions of non-HDL-C (b = 0.785, P = 0.001), non-HDL-C/TC (b = −0.336, P = 0.001) and nonHDL-C/LDL-C (b = 0.295, P = 0.001) influenced AL by 38.6%. The AUC with 95% CI in the high AL group was as follows: non-HDL-C 0.766 (0.696–0.837, P = 0.001); non-HDL-C/HDL-C 0.638 (0.555–0.721, P = 0.002); nonHDL-C/TC 0.635 (0.552–0.712, P = 0.003) and non-HDL-C/LDL-C 0.520 (0.433–0.607, P = 0.657). Non-HDL-C and its fractions were more precisely predicted in the high AL category of workers than in the low AL category. Non-HDL-C predicted the most precisely, followed by non-HDL-C/HDL-C, non-HDL-C/TC, non-HDL-C/ LDL-C and non-HDL-C/TG. Conclusion: According to the present study, non-HDL-C and its fractions such as non-HDL-C/HDL-C, nonHDL-C/TC and non-HDL-C/LDL-C should be considered regular lipid profiles and could be used as biomarkers to reduce the risk of AL.

The mastery lifestyle intervention to reduce biopsychosocial risks for pregnant Latinas and African Americans and their infants: protocol for a randomized controlled trial

BackgroundPregnant Mexican Americans (hereafter called Latinas) and Black/African American women are at increased risk for psychological distress, contributing to preterm birth and low birthweight; acculturative stress combined with perceived stress elevates depressive symptoms in Latinas. Based on our prior research using a psychoneuroimmunology framework, we identified psychological and neuroendocrine risk factors as predictors of preterm birth in Latina women that are also identified as risk factors for Black/African American women.Methods/designIn this prospective, randomized controlled trial with parallel group design we will explore psychosocial, neuroendocrine, and birth outcome effects of the Mastery Lifestyle Intervention (MLI). The MLI is a culturally relevant, manualized, psychosocial, group intervention integrating two cognitive behavioral therapies for both pregnant Latinas and Black/African American women (total n = 221). Study inclusion criteria are: women with current pregnancy at 14–20 weeks gestation, ability to read and speak English or Spanish, self-identify as Latina of Mexican heritage or Black/African American, 18–45 years old, born in the US or Mexico, and currently living in the US. Participants must receive Medicaid or other government-supported insurance, and meet screening criteria for anxiety, depressive symptoms, or stress. Participants are randomly assigned to either the intervention (MLI) or usual care group (UCG) in groups of 6–8 participants that occur over 6 consecutive weeks. Data are collected at 3 time points: enrollment (14–20 weeks gestation), following treatment (20–26 weeks), and 6 weeks after treatment (32–36 weeks gestation). Additional outcome, mediating, and moderating data are collected from the electronic health record during pregnancy and at birth. Analyses will primarily use generalized linear mixed modeling (GLMM) to evaluate the relationships between predictors and outcomes.DiscussionThis RCT will test the efficacy of two combined third generation cognitive behavioral therapies (the MLI), given in a group format over 6 sessions, as compared to a usual prenatal care group, for both Latina and African American pregnant women. If efficacious, it may be provided as an adjunct to routine prenatal care and improve mental health, as well as babies being born too small and too soon.Trial registrationThe trial was retrospectively registered at ClinicalTrials.gov. Bethesda (MD): National Library of Medicine. Identifier NCT05012072, Reducing Pregnancy Risks: The Mastery Lifestyle Intervention (MLI); August 19, 2021. The trial is currently recruiting participants.

Neuroendocrine Blockade of the Reproductive Axis in Female Athletes

This review aims at defining the neuroendocrine mechanisms underlying the sport-induced restrictions of the reproductive axis in female athletes. Episodic gonadotropin release was found to be compromised, presumably a result of impaired hypothalamic pulsatile GnRH release. Any deviation from optimal gonadotropin release may result in a suboptimal function of the ovaries, leading to disorders of the menstrual cycle and ovulation. A whole spectrum of menstrual dysfunctions ranging from ovulatory eumenorrhea to luteal phase defects and amenorrhea has been reported in sportive women. As essential neuroendocrine factors underlying these observations, activation of the adrenal axis and altered central nervous neurotransmitter activity have been identified to transfer metabolic, nutritional, and stress signals into the hypothalamic GnRH release. The degree by which the neuroendocrine axis governing reproduction is impaired critically depends on the intensity and duration of exercise and the state of training. Other decisive factors may be energy expenditure and availability, nutritional components, and the maturity of the hypothalamic-pituitary-ovarian (HPO) axis when sport activity was initiated. In conclusion, the gradual cessation of reproductive function observed in female athletes may be interpreted as an adaptive mechanism in response to physical and psychological endurance during sport. This sport-induced restriction of reproductive capacity may serve as protection (endogenous contraception) to preserve a woman’s health.

Cardiometabolic consequences of PCOS

Polycystic ovary syndrome (PCOS) is a heterogeneous disorder in terms of clinical symptoms and laboratory findings. It is one of the most common endocrinopathies in women of childbearing age. The development of symptoms and the degree of severity in the course of the disease are the results of changes in the ovaries which may be caused by many genetic, metabolic, neuroendocrine, and environmental factors. The main clinical manifestations are menstrual disorders, difficulties with becoming pregnant, and changes related to hyperandrogenism, e.g., acne, hirsutism. Recognition is above mainly based on Rotterdam criteria.A comprehensive explanation of pathophysiology is still lacking. Nevertheless, it probably is a multifactorial condition with a genetic component. Women suffering from PCOS experience lipid and carbohydrate metabolism disorders, which lead to insulin resistance, obesity, hypertension, and cardiac complications. Insulin resistance affects 65-70% of women and not only plays a significant role in the development of the disease but also contributes to the development of hypertension and dyslipidemia. Potential mechanisms of hypertension in PCOS include endothelial dysfunction, increased aldosterone, and excess testosterone secretion, whereas lipid abnormalities consist of reduced high-density lipoprotein-cholesterol (HDL-C), increased triglycerides, and low-density lipoprotein-cholesterol (LDL-C). All of these factors cause high cardiovascular risk. Currently, therapy considers both lifestyle improvements and medications and must be tailored on a case-by-case basis. It is very important not to consider PCOS only in the context of gynecological and endocrine diseases, but also metabolic changes and cardiovascular diseases. Treatment of PCOS should be individualized and dependent on the predominant disorders, as well as the short- and long-term goals chosen. It also should take the prevention of cardiovascular diseases into account.

Current Perspectives of Neuroendocrine Regulation in Liver Fibrosis.

Liver fibrosis is a complicated process that involves different cell types and pathological factors. The excessive accumulation of extracellular matrix (ECM) and the formation of fibrotic scar disrupt the tissue homeostasis of the liver, eventually leading to cirrhosis and even liver failure. Myofibroblasts derived from hepatic stellate cells (HSCs) contribute to the development of liver fibrosis by producing ECM in the area of injuries. It has been reported that the secretion of the neuroendocrine hormone in chronic liver injury is different from a healthy liver. Activated HSCs and cholangiocytes express specific receptors in response to these neuropeptides released from the neuroendocrine system and other neuroendocrine cells. Neuroendocrine hormones and their receptors form a complicated network that regulates hepatic inflammation, which controls the progression of liver fibrosis. This review summarizes neuroendocrine regulation in liver fibrosis from three aspects. The first part describes the mechanisms of liver fibrosis. The second part presents the neuroendocrine sources and neuroendocrine compartments in the liver. The third section discusses the effects of various neuroendocrine factors, such as substance P (SP), melatonin, as well as α-calcitonin gene-related peptide (α-CGRP), on liver fibrosis and the potential therapeutic interventions for liver fibrosis.

CNSC-09. THE NEUROENDOCRINE FACTOR VGF IS NECESSARY FOR THE MAINTENANCE OF THE TUMOR STEM CELL POPULATION IN GLIOBLASTOMA

Abstract A major factor that contributes to the unchecked growth and recurrence of glioblastoma (GBM) tumors is the presence of a heterogeneous population of GBM stem-like cells (GSCs) that continuously replenish the tumor mass. Targeting strategies against this key cell population have rarely considered the trophic signals from peritumoral neural cells, which can protect the tumor cells during therapy and therefore promote recurrence. Here, we have focused on the little-known secreted factor VGF and its derived neuropeptides, which are largely restricted to the CNS and mediate paracrine communication between neural cells. We analyzed over 200 tissue specimens and cultured GBM cells, demonstrating that VGF is upregulated in malignant gliomas and expressed in GSCs of different subtypes, although it is markedly reduced in differentiated GBM cells. More importantly, we detected VGF expression in peritumoral astrocytes, even though this neuroendocrine factor has never been described in glial cells in normal brain. Co-culture experiments and scRNAseq data from clinical tumors confirmed that VGF is expressed in tumor-associated astrocytes, suggesting that these cells are a paracrine source of VGF in GBM. Accordingly, purified exogenous VGF increased the proliferation of GSCs and rescued GSC viability when the tumor cells were treated with the chemotherapeutic temozolomide. Moreover, purified VGF decreased the expression of inflammatory cytokines in activated macrophages, suggesting that this factor may also contribute to local immunosuppression in gliomas. Conversely, knockdown of VGF in GSCs was sufficient to decrease their viability, self-renewal, and expression of stemness-related genes. At the molecular level, VGF increased intracellular calcium and Akt/mTOR signaling in GSCs, suggesting a possible G protein coupled receptor-mediated mechanism of action. Taken together, our results explore for the first time the role of brain-derived VGF in GBM progression, highlighting the importance of disrupting the communication between the tumor and its microenvironment to achieve long-term anti-tumor efficacy.

Impact of Physiologically Relevant Genistein Exposure at Different Time Windows on Puberty Onset and Neuroendocrine Function in Female Rats.

Puberty timing, critical for adulthood wellbeing, is influenced by the environment, life-style, and diets. However, differential puberty-interfering effects of soy and soy isoflavone are observed in both epidemiological and toxicological studies. Additionally, their impact on neuroendocrine function at various pre-pubertal developmental windows is unclear. This study investigates the effect of genistein, a typical soy isoflavone, at neonatal, lactational, and post-weaning stages on the time of vaginal opening and determines the levels of neuroendocrine factors in female rats using immunofluorescence, immunochemistry, and enzyme-linked immunosorbent assays. A physiologically relevant dosage (10mgkg-1 ) is used to resemble human exposure. The results show that genistein exposure at lactational stage significantly accelerates vaginal opening time, marginally increases hypothalamic gonadotropin-releasing hormone (GnRH) secretion, significantly enhances kisspeptin receptor expression, and markedly elevates blood levels of GnRH, luteinizing hormone, and follicle-stimulating hormone, while neonatal and post-weaning exposures do not induce significant alternations. Lactational stage may be an important window for genistein to impact reproductive development and neuroendocrine regulations.

Molecular Mechanisms Linking Inflammation to Autoimmunity in Sjögren's Syndrome: Identification of New Targets.

Sjögren's syndrome (SS) is a systemic autoimmune rheumatic disorder characterized by the lymphocytic infiltration of exocrine glands and the production of autoantibodies to self-antigens. The involvement of the exocrine glands drives the pathognomonic manifestations of dry eyes (keratoconjunctivitis sicca) and dry mouth (xerostomia) that define sicca syndrome. To date, the molecular mechanisms mediating pathological salivary gland dysfunction in SS remain to be elucidated, despite extensive studies investigating the underlying cause of this disease, hampering the development of novel therapeutic strategies. Many researchers have identified a multifactorial pathogenesis of SS, including environmental, genetic, neuroendocrine, and immune factors. In this review, we explore the latest developments in understanding the molecular mechanisms involved in the pathogenesis of SS, which have attracted increasing interest in recent years.

Individualities mediate divergent stress responses and appetite regulation in CNS of olive flounder, Paralichthys olivaceus

In farmed animals, individualities have demonstrated links to health and welfare. However, differential modulation of orexigenic, anorexigenic neuroendocrine and endocrine factors in different individuals with different individualities remain unclear. Therefore, we investigated the contribution of the hypothalamic-pituitary-interrenal (HPI), anorexigenic and orexigenic signal molecules to the regulation of appetite in different individuals of adult olive flounder exposed to social isolation stress. We employed behavior assays to separate flounder into three behavioural types (proactive- 14%, intermediate- 30% and reactive- 56%). We found marked elevation in plasma corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH) and cortisol, and a stronger suppression of feeding post-stress in reactive than other groups. Reactive also had significantly higher CRH and urotensin (UI) mRNA levels in the preoptic area, hypothalamus, hind brain, spinal cord and caudal neurosecretory system (CNSS) than the rest of the groups. Similarly, brain anorexigenic cholecystokinin (CCK), serotonin (5-HT1A) and glucocorticoid receptor (GR) mRNA levels in the preoptic area, telencephalon, hypothalamus, hind brain and CNSS were all higher in reactive than other groups. Contrary, reactive had lower neuropeptide Y (NPY), ghrelin and prolactin mRNA levels in the preoptic area, telencephalon, hypothalamus and CNSS than other groups. There was no significant difference between proactive and intermediate in all measured parameters. Overall, the results demonstrate that social isolation stress is differentially modulated in different individuals and those CRH-related peptides, anorexigenic and orexigenic signalling molecules contribute to divergent stress response and regulation of appetite in P. olivaceus.

Roles of traditional chinese medicine regulating neuroendocrinology on AD treatment.

The incidence of sporadic Alzheimer’s disease (AD) is increasing in recent years. Studies have shown that in addition to some genetic abnormalities, the majority of AD patients has a history of long-term exposure to risk factors. Neuroendocrine related risk factors have been proved to be strongly associated with AD. Long-term hormone disorder can have a direct detrimental effect on the brain by producing an AD-like pathology and result in cognitive decline by impairing neuronal metabolism, plasticity and survival. Traditional Chinese Medicine(TCM) may regulate the complex process of endocrine disorders, and improve metabolic abnormalities, as well as the resulting neuroinflammation and oxidative damage through a variety of pathways. TCM has unique therapeutic advantages in treating early intervention of AD-related neuroendocrine disorders and preventing cognitive decline. This paper reviewed the relationship between neuroendocrine and AD as well as the related TCM treatment and its mechanism. The advantages of TCM intervention on endocrine disorders and some pending problems was also discussed, and new insights for TCM treatment of dementia in the future was provided.

Endocrine-Disrupting Chemicals Exposure Alter Neuroendocrine Factors, Disrupt Cardiac Functions and Provokes Hypoxia Conditions in Zebrafish Model.

Zebrafish (Danio rerio) is an increasingly popular vertebrate model used for assessing the toxicity of endocrine-disrupting chemicals (EDCs) on living beings. The zebrafish features high genetic homology to mammals, because of its rapid embryonic development, optical transparency of phenotypic screening embryos, high throughput genetic and chemical screening which make them a powerful toxicological model. This systematic review aimed to assess the recent literature on the use of zebrafish model in EDCs toxicity studies. We capture the data on the types of EDCs used, zebrafish life stages associated with the toxicity, and its effects on the alterations in neuroendocrine factors and cardiac hypoxia in zebrafish. A total of 17 articles published between 2010 and 2020 were curated. The information gathered highlighted the association of EDCs with cardiological outcomes and neurobehavioral effects and distorted expression of genes. The genes that were highlighted in the paper include bdnf, ntrk2a, grin2cb, VTG-1, HIF-1α, tnnt2, ntrk1, and pax6b. The effect of EDCs on cardiac hypoxia and neurodevelopmental and behavioral factors of zebrafish were described in all the papers chosen for this review. The involvement of EDCs in altered regulation of gene expression can be studied further to identify the potential EDC compounds on its toxicological and endocrine disruption function at the molecular level.