Suicide, Serotonin, and the Brain

Crisis ◽  
2001 ◽  
Vol 22 (2) ◽  
pp. 66-70 ◽  
Author(s):  
C. van Heeringen
Keyword(s):  
Suicidal Behavior ◽  
Behavioral Inhibition ◽  
Biological Psychiatry ◽  
Future Research ◽  
Research Findings ◽  
The Central Nervous System ◽  
Serotonergic Function ◽  
The Brain ◽  
Serotonergic Dysfunction

Summary: The involvement of impaired serotonergic functioning in the development of suicidal behavior is one of the best documented findings in biological psychiatry. It is, however, less clear in which way this dysfunction contributes to the occurrence of suicidal behavior. Correlational studies have demonstrated associations between peripheral measures of serotonergic function and characteristics such as impulsivity, disinhibition, anxiety, and/or behavioral inhibition. Postmortem and neuroimaging studies have provided insight in the localization of serotonergic dysfunction in the central nervous system. Nevertheless, results in this area of research have also been contradictory. Following a short overview of recent research findings on serotonin and suicidal behavior, this paper focuses on the involvement of the prefrontal cortex of the brain in the development of suicidal behavior and on the role of serotonin in its executive functions. Based on these considerations, suggestions for future research are discussed.

Neuropeptides and anxiety disorders

1992 ◽  
Vol 4 (2) ◽  
pp. 25-30 ◽  
Author(s):  
H.J.G.M. van Megen ◽  
J.A. den Boer ◽  
H.G.M. Westenberg
Keyword(s):  
Anxiety Disorders ◽  
Animal Experiments ◽  
Future Research ◽  
Working Mechanism ◽  
Animal Data ◽  
Research Findings ◽  
Relationship Of ◽  
The Relationship ◽  
The Brain

SummaryIn this review article four neuropeptides: adrenocorticotrope hormone (ACTH), corticotrope releasing hormone (CRH), neuropeptide- Y(NPY) and cholecystokinin (CCK) are discussed with respect to their possible role in the pathogenesis of anxiety disorders. First the presumable working mechanism of these peptides in the brain is mentioned. In addition, the relationship of these peptides and anxiety is outlined using neuroanatomical and electrophysiological research data. Subsequently, animal experiments and human research findings are discussed. Most of the research findings so far are obtained from animal data. Only with respect to CCK, there is increasing evidence, also from human studies, that this peptide might play a role in the pathogenesis of anxiety disorders. The putative role of the other peptides remains to be estab lished in future research.

scholarly journals The Microbiota–Gut–Brain Axis and Alzheimer Disease. From Dysbiosis to Neurodegeneration: Focus on the Central Nervous System Glial Cells

2021 ◽  
Vol 10 (11) ◽  
pp. 2358
Author(s):  
Maria Grazia Giovannini ◽  
Daniele Lana ◽  
Chiara Traini ◽  
Maria Giuliana Vannucchi
Keyword(s):  
Alzheimer Disease ◽  
Glial Cells ◽  
Cell Types ◽  
The Past ◽  
The Central Nervous System ◽  
Diseased State ◽  
The Brain ◽  
Alzheimer Disease Pathogenesis ◽  
Brain Homeostasis

The microbiota–gut system can be thought of as a single unit that interacts with the brain via the “two-way” microbiota–gut–brain axis. Through this axis, a constant interplay mediated by the several products originating from the microbiota guarantees the physiological development and shaping of the gut and the brain. In the present review will be described the modalities through which the microbiota and gut control each other, and the main microbiota products conditioning both local and brain homeostasis. Much evidence has accumulated over the past decade in favor of a significant association between dysbiosis, neuroinflammation and neurodegeneration. Presently, the pathogenetic mechanisms triggered by molecules produced by the altered microbiota, also responsible for the onset and evolution of Alzheimer disease, will be described. Our attention will be focused on the role of astrocytes and microglia. Numerous studies have progressively demonstrated how these glial cells are important to ensure an adequate environment for neuronal activity in healthy conditions. Furthermore, it is becoming evident how both cell types can mediate the onset of neuroinflammation and lead to neurodegeneration when subjected to pathological stimuli. Based on this information, the role of the major microbiota products in shifting the activation profiles of astrocytes and microglia from a healthy to a diseased state will be discussed, focusing on Alzheimer disease pathogenesis.

scholarly journals Involvement of Microglia in the Pathophysiology of Intracranial Aneurysms and Vascular Malformations—A Short Overview

2021 ◽  
Vol 22 (11) ◽  
pp. 6141
Author(s):  
Teodora Larisa Timis ◽  
Ioan Alexandru Florian ◽  
Sergiu Susman ◽  
Ioan Stefan Florian
Keyword(s):  
Immune Cells ◽  
Arteriovenous Malformations ◽  
Intracranial Aneurysms ◽  
Immune Cell ◽  
Vascular Malformations ◽  
Cerebral Injury ◽  
Future Research ◽  
Mortality And Morbidity ◽  
The Central Nervous System ◽  
The Brain

Aneurysms and vascular malformations of the brain represent an important source of intracranial hemorrhage and subsequent mortality and morbidity. We are only beginning to discern the involvement of microglia, the resident immune cell of the central nervous system, in these pathologies and their outcomes. Recent evidence suggests that activated proinflammatory microglia are implicated in the expansion of brain injury following subarachnoid hemorrhage (SAH) in both the acute and chronic phases, being also a main actor in vasospasm, considerably the most severe complication of SAH. On the other hand, anti-inflammatory microglia may be involved in the resolution of cerebral injury and hemorrhage. These immune cells have also been observed in high numbers in brain arteriovenous malformations (bAVM) and cerebral cavernomas (CCM), although their roles in these lesions are currently incompletely ascertained. The following review aims to shed a light on the most significant findings related to microglia and their roles in intracranial aneurysms and vascular malformations, as well as possibly establish the course for future research.

The role of tryptophan in hepatic encephalopathy

1993 ◽  
Vol 5 (4) ◽  
pp. 71-75
Author(s):  
C. Aaldijk ◽  
W.W. Van Den Broek ◽  
R.C. Van Der Mast
Keyword(s):  
Hepatic Encephalopathy ◽  
Clinical Picture ◽  
Serotonergic System ◽  
Pathogenetic Mechanisms ◽  
Research Findings ◽  
Glutamine Synthesis ◽  
The Brain ◽  
Tryptophan Uptake

SummaryIn this review the most important hypotheses for the occurrence of the clinical picture of hepatic encephalopathy are discussed. As possible pathogenetic mechanisms are raised: dysfunction of the serotonergic system due to an increased tryptophan uptake in the brain, an elevated intracerebral ammoniac concentration and glutamine synthesis, and a heightened intracerebral GABA-activity.The dysregulation of the serotonergic system as a consequence of the increased intracerebral tryptophan uptake is described as one of the most important pathogenetic mechanisms. The elevated intracerebral ammoniac concentration and the elevated intracerebral glutamine synthesis play in this a facilitating role. The similarity in symptomatology of the clinical picture of HE and the serotonergic syndrome support this hypothesis. Due to contradictory research findings the role of the GABA-ergic system and the occurrence of HE remains unclear.

The Advancement of Neuroimaging Research Investigating Developmental Stuttering

2011 ◽  
Vol 21 (3) ◽  
pp. 88-95 ◽  
Author(s):  
Deryk S. Beal
Keyword(s):  
Speech Production ◽  
Fast Rate ◽  
Neural Correlates ◽  
Future Research ◽  
Current State ◽  
Developmental Stuttering ◽  
The Brain ◽  
State Of The Field

We are amassing information about the role of the brain in speech production and the potential neural limitations that coincide with developmental stuttering at a fast rate. As such, it is difficult for many clinician-scientists who are interested in the neural correlates of stuttering to stay informed of the current state of the field. In this paper, I aim to inspire clinician-scientists to tackle hypothesis-driven research that is grounded in neurobiological theory. To this end, I will review the neuroanatomical structures, and their functions, which are implicated in speech production and then describe the relevant differences identified in these structures in people who stutter relative to their fluently speaking peers. I will conclude the paper with suggestions on directions of future research to facilitate the evolution of the field of neuroimaging of stuttering.

Neurotrophins and Proneurotrophins: Focus on Synaptic Activity and Plasticity in the Brain

2017 ◽  
Vol 23 (6) ◽  
pp. 587-604 ◽  
Author(s):  
Julien Gibon ◽  
Philip A. Barker
Keyword(s):  
Long Term Potentiation ◽  
Synaptic Activity ◽  
Cellular Processes ◽  
Term Potentiation ◽  
Neurotrophin 3 ◽  
New Findings ◽  
The Central Nervous System ◽  
The Brain

Neurotrophins have been intensively studied and have multiple roles in the brain. Neurotrophins are first synthetized as proneurotrophins and then cleaved intracellularly and extracellularly. Increasing evidences demonstrate that proneurotrophins and mature neurotrophins exerts opposing role in the central nervous system. In the present review, we explore the role of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin 3 (NT3), and neurotrophin 4 (NT4) and their respective proform in cellular processes related to learning and memory. We focused on their roles in synaptic activity and plasticity in the brain with an emphasis on long-term potentiation, long-term depression, and basal synaptic transmission in the hippocampus and the temporal lobe area. We also discuss new findings on the role of the Val66Met polymorphism on the BDNF propeptide on synaptic activity.

scholarly journals Glymphatic System in the Central Nervous System, a Novel Therapeutic Direction Against Brain Edema After Stroke

2021 ◽  
Vol 13 ◽  
Author(s):  
Xiangyue Zhou ◽  
Youwei Li ◽  
Cameron Lenahan ◽  
Yibo Ou ◽  
Minghuan Wang ◽  
...  
Keyword(s):  
Brain Edema ◽  
Brain Tissue ◽  
Molecular Mechanisms ◽  
Glymphatic System ◽  
System A ◽  
Function Recovery ◽  
The Central Nervous System ◽  
The Stability ◽  
The Brain

Stroke is the destruction of brain function and structure, and is caused by either cerebrovascular obstruction or rupture. It is a disease associated with high mortality and disability worldwide. Brain edema after stroke is an important factor affecting neurologic function recovery. The glymphatic system is a recently discovered cerebrospinal fluid (CSF) transport system. Through the perivascular space and aquaporin 4 (AQP4) on astrocytes, it promotes the exchange of CSF and interstitial fluid (ISF), clears brain metabolic waste, and maintains the stability of the internal environment within the brain. Excessive accumulation of fluid in the brain tissue causes cerebral edema, but the glymphatic system plays an important role in the process of both intake and removal of fluid within the brain. The changes in the glymphatic system after stroke may be an important contributor to brain edema. Understanding and targeting the molecular mechanisms and the role of the glymphatic system in the formation and regression of brain edema after stroke could promote the exclusion of fluids in the brain tissue and promote the recovery of neurological function in stroke patients. In this review, we will discuss the physiology of the glymphatic system, as well as the related mechanisms and therapeutic targets involved in the formation of brain edema after stroke, which could provide a new direction for research against brain edema after stroke.

scholarly journals Role of Immunity in Pathogenesis of Psychosis

2021 ◽  
Author(s):  
Wafa Abdelghaffar ◽  
Oussama Sidhom ◽  
Lilia Laadhar ◽  
Rym Rafrafi
Keyword(s):  
Mental Health ◽  
Immune System ◽  
Psychiatric Symptoms ◽  
Scientific Evidence ◽  
Health Conditions ◽  
Future Research ◽  
Antineuronal Antibodies ◽  
System Components ◽  
The Brain

The involvement of immunity in the pathogenesis of schizophrenia and related psychoses was suspected a century ago but was shadowed by the dopaminergic hypothesis after the discovery of antipsychotics. We currently know that this latter theory has many limits and cannot account for the wide variety of psychotic conditions. The immune-inflammatory theory is now one of the most promising axes of research in terms of pathogenesis of several mental health conditions. Immunity and inflammation play a role at least in a subgroup of patients with psychosis. The immune system is complex with a variety of components and mediators that can all have effects on the brain and thus mediate psychiatric symptoms. In this chapter we will explore the scientific evidence of the role of immune system in pathophysiology of psychosis. The sections of this chapter will discuss the role of innate system components (cytokines, microglia, inflammation.), the role of adaptive system (lymphocytes and antibodies) with a section focusing on auto-immunity and particularly antineuronal antibodies. Finally we will discuss how this research can impact patients management and elaborate recommendations for future research.

Сellular and Molecular Mechanisms of Proinflammatory Monocytes Participation in the Pathogenesis of Mental Disorders. Part 3

Psychiatry ◽  
2021 ◽  
Vol 19 (4) ◽  
pp. 125-134
Author(s):  
E. F. Vasilyeva ◽  
O. S. Brusov
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Mental Disorders ◽  
Molecular Mechanisms ◽  
Microglial Cells ◽  
Inflammatory Reactions ◽  
Mental Diseases ◽  
The Central Nervous System ◽  
The Brain

Background: at present, the important role of the monocyte-macrophage link of immunity in the pathogenesis of mental diseases has been determined. In the first and second parts of our review, the cellular and molecular mechanisms of activation of monocytes/macrophages, which secreting proinflammatory CD16 receptors, cytokines, chemokines and receptors to them, in the development of systemic immune inflammation in the pathogenesis of somatic diseases and mental disorders, including schizophrenia, bipolar affective disorder (BAD) and depression were analyzed. The association of high levels of proinflammatory activity of monocytes/macrophages in patients with mental disorders with somatic comorbidity, including immune system diseases, is shown. It is known that proinflammatory monocytes of peripheral blood, as a result of violation of the integrity of the hematoencephalic barrier can migrate to the central nervous system and activate the resident brain cells — microglia, causing its activation. Activation of microglia can lead to the development of neuroinammation and neurodegenerative processes in the brain and, as a result, to cognitive disorders. The aim of review: to analyze the results of the main scientific studies concerning the role of cellular and molecular mechanisms of peripheral blood monocytes interaction with microglial cells and platelets in the development of neuroinflammation in the pathogenesis of mental disorders, including Alzheimer’s disease (AD). Material and methods: keywords “mental disorders, AD, proinflammatory monocytes, microglia, neuroinflammation, cytokines, chemokines, cell adhesion molecules, platelets, microvesicles” were used to search for articles of domestic and foreign authors published over the past 30 years in the databases PubMed, eLibrary, Science Direct and EMBASE. Conclusion: this review analyzes the results of studies which show that monocytes/macrophages and microglia have similar gene expression profiles in schizophrenia, BAD, depression, and AD and also perform similar functions: phagocytosis and inflammatory responses. Monocytes recruited to the central nervous system stimulate the increased production of proinflammatory cytokines IL-1, IL-6, tumor necrosis factor alpha (TNF-α), chemokines, for example, MCP-1 (Monocyte chemotactic protein-1) by microglial cells. This promotes the recruitment of microglial cells to the sites of neuronal damage, and also enhances the formation of the brain protein beta-amyloid (Aβ). The results of modern studies are presented, indicating that platelets are involved in systemic inflammatory reactions, where they interact with monocytes to form monocyte-platelet aggregates (MTA), which induce the activation of monocytes with a pro inflammatory phenotype. In the last decade, it has been established that activated platelets and other cells of the immune system, including monocytes, detached microvesicles (MV) from the membrane. It has been shown that MV are involved as messengers in the transport of biologically active lipids, cytokines, complement, and other molecules that can cause exacerbation of systemic inflammatory reactions. The presented review allows us to expand our knowledge about the cellular and molecular aspects of the interaction of monocytes/macrophages with microglial cells and platelets in the development of neuroinflammation and cognitive decline in the pathogenesis of mental diseases and in AD, and also helps in the search for specific biomarkers of the clinical severity of mental disorder in patients and the prospects for their response to treatment.

Conclusion and Recommendations

2014 ◽  
pp. 226-238
Keyword(s):  
Economic Growth ◽  
Growth Process ◽  
Financial Sector ◽  
Policy Implications ◽  
Future Research ◽  
Financial Sector Development ◽  
Research Findings ◽  
Potential Channels

This book started with a brief review of different outlooks on the role of financial sector development in the process of economic growth. Then it highlighted the fact that recent studies, particularly those originating from modern growth theory, suggest that financial intermediation affects growth through various channels. To test this proposition, an empirical model was built, data were obtained, empirical tests were carried out, and results were discussed. The final chapter in this book, therefore, summarises key research findings and discusses the potential channels through which financial sector development affects the economic growth process. The chapter further highlights contributions of this research to growth studies, discusses policy implications arising from the findings of this research, and provides directions for future research and analysis.

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