scholarly journals Regulation of the Brain Neural Niche by Soluble Molecule Akhirin

2021 ◽  
Vol 9 (3) ◽  
pp. 29
Author(s):  
Mikiko Kudo ◽  
Kunimasa Ohta
Keyword(s):  
Spinal Cord ◽  
Blood Vessels ◽  
Molecular Mechanisms ◽  
Neural Progenitor Cells ◽  
Central Canal ◽  
Neural Cells ◽  
Neural Tissues ◽  
The Central Nervous System ◽  
The Brain

In the central nervous system (CNS), which comprises the eyes, spinal cord, and brain, neural cells are produced by the repeated division of neural stem cells (NSCs) during the development of the CNS. Contrary to the notion that the CNS is relatively static with a limited cell turnover, cells with stem cell-like properties have been isolated from most neural tissues. The microenvironment, also known as the NSC niche, consists of NSCs/neural progenitor cells, other neurons, glial cells, and blood vessels; this niche is thought to regulate neurogenesis and the differentiation of NSCs into neurons and glia. Although it has been established that neurons, glia, and blood vessels interact with each other in a complex manner to generate neural tissues in the NSC niche, the underlying molecular mechanisms in the CNS niche are unclear. Herein, we would like to introduce the extracellular secreted protein, Akhirin (AKH; Akhi is the Bengali translation for eye). AKH is specifically expressed in the CNS niche—the ciliary body epithelium in the retina, the central canal of the spinal cord, the subventricular zone, and the subgranular zone of the dentate gyrus of the hippocampus—and is supposedly involved in NSC niche regulation. In this review, we discuss the role of AKH as a niche molecule during mouse brain formation.

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.

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.

scholarly journals Methamphetamine-Triggered Neurotoxicity in Human Dorsolateral Prefrontal Cortex

2021 ◽  
Vol 10 ◽  
pp. 2016
Author(s):  
Ali Zare ◽  
Alireza Ghanbari ◽  
Mohammad Javad Hoseinpour ◽  
Mahdi Eskandarian Boroujeni ◽  
Alimohammad Alimohammadi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Prefrontal Cortex ◽  
Dorsolateral Prefrontal Cortex ◽  
Animal Studies ◽  
Molecular Mechanisms ◽  
Metabolic Activation ◽  
Neural Cells ◽  
Dorsolateral Prefrontal ◽  
The Central Nervous System ◽  
The Brain

Background: Methamphetamine (MA), is an extremely addictive stimulant that adversely affects the central nervous system. Accumulating evidence indicates that molecular mechanisms such as oxidative stress, apoptosis, and autophagy are involved in the toxicity of MA. Considering experimental animal studies exhibiting MA-induced neurotoxicity, the relevance of these findings needs to be evidently elucidated in human MA users. It is generally assumed that multiple chemical substances released in the brain following MA-induced metabolic activation are primary factors underlying damage of neural cells. Hence, this study aimed to investigate the role of autophagy and apoptosis as well as oxidative stress in the brain of postmortem MA-induced toxicity. Materials and Methods: In this study, we determine the gene expression of autophagy and apoptosis, including BECN1, MAP1ALC3, CASP8, TP53, and BAX genes in ten healthy controls and ten chronic users of MA postmortem dorsolateral prefrontal cortex (DLPFC) by real-time polymerase chain reaction. Also, we applied immunohistochemistry in formalin-fixed and paraffin-embedded human brain samples to analyze brain-derived neurotrophic factor (BDNF). Also, spectrophotometry was performed to measure glutathione (GSH) content. Results: The expression level of apoptotic and autophagic genes (BECN1, MAP1ALC3, CASP8, TP53, and BAX) were significantly elevated, while GSH content and BDNF showed substantial reductions in DLPFC of chronic MA users. Discussion: Our data showed that MA addiction provokes transduction pathways, namely apoptosis and autophagy, along with oxidative mechanisms in DLPFC. Also, MA induces multiple functional and structural perturbations in the brain, determining its toxicity and possibly contributing to neurotoxicity. [GMJ.2021;10:e2016]

scholarly journals Cross-talk between blood vessels and neural progenitors in the developing brain

2018 ◽  
Vol 2 (1) ◽  
Author(s):  
Mathew Tata ◽  
Christiana Ruhrberg
Keyword(s):  
Nervous System ◽  
Blood Vessels ◽  
Cross Talk ◽  
Neural Progenitor Cells ◽  
Vascular Supply ◽  
Neural Cells ◽  
Reciprocal Regulation ◽  
Genetic Manipulations ◽  
Vessel Growth ◽  
The Central Nervous System

The formation of the central nervous system (CNS) involves multiple cellular and molecular interactions between neural progenitor cells (NPCs) and blood vessels to establish extensive and complex neural networks and attract a vascular supply that support their function. In this review, we discuss studies that have performed genetic manipulations of chick, fish and mouse embryos to define the spatiotemporal roles of molecules that mediate the reciprocal regulation of NPCs and blood vessels. These experiments have highlighted core functions of NPC-expressed ligands in initiating vascular growth into and within the neural tube as well as establishing the blood–brain barrier. More recent findings have also revealed indispensable roles of blood vessels in regulating NPC expansion and eventual differentiation, and specific regional differences in the effect of angiocrine signals. Accordingly, NPCs initially stimulate blood vessel growth and maturation to nourish the brain, but blood vessels subsequently also regulate NPC behaviour to promote the formation of a sufficient number and diversity of neural cells. A greater understanding of the molecular cross-talk between NPCs and blood vessels will improve our knowledge of how the vertebrate nervous system forms and likely help in the design of novel therapies aimed at regenerating neurons and neural vasculature following CNS disease or injury.

scholarly journals Steroids, spinal cord and pain sensation

2011 ◽  
Vol 7 (3) ◽  
Author(s):  
Christine Patte-Mensah ◽  
Laurence Meyer ◽  
Ayikoe Guy Mensah-Nyagan
Keyword(s):  
Spinal Cord ◽  
Nervous System ◽  
Pain Modulation ◽  
Pain Sensation ◽  
Effective Strategies ◽  
Neural Tissues ◽  
The Central Nervous System ◽  
Regulatory Effects ◽  
Hormonal Steroids ◽  
The Brain

AbstractDuring the whole life, the nervous system is continuously submitted to the actions of different categories of hormones, including steroids. Therefore, the interactions between hormonal compounds and neural tissues are subjected to intense investigations. While a majority of studies focus on the brain, the spinal cord (SC) has received little attention, although this structure is also an important part of the central nervous system, controlling motor and sensory functions. To point out the importance of interactions between hormones and the SC in the regulation of neurobiological activities, we recapitulated and discussed herein various key data, revealing that the pivotal role played by the SC in nociception and pain modulation, directly depends on the SC ability to metabolize and synthesize steroidal molecules. The paper suggests that future investigations aiming to develop effective strategies against chronic pain, must integrate regulatory effects exerted by hormonal steroids on the SC activity, as well as the actions of endogenous neurosteroids locally synthesized in spinal neural networks.

BIOLOGICAL ROLE OF ERYTHROPOIETIN IN THE PERINATAL PERIOD: NON-ERYTHROPOIETIC FUNCTIONS IN HYPOXIC-ISCHEMIC LESIONS OF THE CENTRAL NERVOUS SYSTEM

2021 ◽  
Vol 100 (1) ◽  
pp. 83-89
Author(s):  
S.B. Berezhanskaya ◽  
◽  
E.A. Lukianova ◽  
M.K. Abduragimova ◽  
◽  
...  
Keyword(s):  
Spinal Cord ◽  
Growth And Development ◽  
Biological Significance ◽  
Perinatal Period ◽  
Critical Conditions ◽  
Ischemic Damage ◽  
The Central Nervous System ◽  
Brain And Spinal Cord ◽  
The Brain

Erythropoietin is recognized as a pluripotent glycoprotein with unique biochemical and epigenetic properties that are important for fetal growth and development, as well as in critical conditions in subsequent periods of ontogenesis. In recent decades, researchers and clinicians have increased interest in the problem of the biological significance of erythropoietin, which can form the basis for constructing algorithms for early prognosis and diagnosis, optimizing the treatment of pathology of the perinatal period, including perinatal hypoxic-ischemic damage to the brain and spinal cord, which are at risk of disability and have a risk of disability significant role in neonatology and perinatal neurology.

Brain and mind

2001 ◽  
Vol 9 (4) ◽  
pp. 389-398 ◽  
Author(s):  
EDOARDO BONCINELLI
Keyword(s):  
Brain Evolution ◽  
Neural Cells ◽  
Research Strategies ◽  
Evolution And Development ◽  
Biological Studies ◽  
The Central Nervous System ◽  
The Subject ◽  
The Brain ◽  
Remote Past

We are beginning to understand how the brain is organized and works, how it evolved in the remote past and how it continually forms during the embryonic development of individual organisms. The study of the brain and its activity has recently advanced at an accelerating pace thanks to the convergence of a number of research strategies. At least three research lines occupy a particular position among these strategies: genetics and the molecular biology of neural cells and the central nervous system; cognitive science; and brain imaging. If the brain is the subject of biological studies at the cellular, intercellular and circuitry levels, the approach to the study of mind should be more subtle. Nonetheless, science has progressed a long way in this direction. Some recent advances in this field are briefly reviewed here, with particular emphasis on brain evolution and development, the role of sensory organs, coding and the processing of sensorial information, memory, rationality, meaning and consciousness.

Central Nerve System Impairment, AMA Guides, Sixth Edition: An Overview

2018 ◽  
Vol 23 (1) ◽  
pp. 10-13
Author(s):  
James B. Talmage ◽  
Jay Blaisdell
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Neurological Impairment ◽  
Sixth Edition ◽  
Central Nerve System ◽  
The Central Nervous System ◽  
The One ◽  
Nerve System ◽  
The Brain

Abstract Injuries that affect the central nervous system (CNS) can be catastrophic because they involve the brain or spinal cord, and determining the underlying clinical cause of impairment is essential in using the AMA Guides to the Evaluation of Permanent Impairment (AMA Guides), in part because the AMA Guides addresses neurological impairment in several chapters. Unlike the musculoskeletal chapters, Chapter 13, The Central and Peripheral Nervous System, does not use grades, grade modifiers, and a net adjustment formula; rather the chapter uses an approach that is similar to that in prior editions of the AMA Guides. The following steps can be used to perform a CNS rating: 1) evaluate all four major categories of cerebral impairment, and choose the one that is most severe; 2) rate the single most severe cerebral impairment of the four major categories; 3) rate all other impairments that are due to neurogenic problems; and 4) combine the rating of the single most severe category of cerebral impairment with the ratings of all other impairments. Because some neurological dysfunctions are rated elsewhere in the AMA Guides, Sixth Edition, the evaluator may consult Table 13-1 to verify the appropriate chapter to use.

scholarly journals Spinal vertebrae localization and analysis on disproportionality in curvature using radiography—a comprehensive review

2021 ◽  
Vol 2021 (1) ◽  
Author(s):  
Joddat Fatima ◽  
Muhammad Usman Akram ◽  
Amina Jameel ◽  
Adeel Muzaffar Syed
Keyword(s):  
Spinal Cord ◽  
Template Matching ◽  
Human Anatomy ◽  
Comprehensive Overview ◽  
Low Contrast ◽  
Active Shape Models ◽  
Harris Corner ◽  
Illumination Changes ◽  
The Central Nervous System ◽  
The Brain

AbstractIn human anatomy, the central nervous system (CNS) acts as a significant processing hub. CNS is clinically divided into two major parts: the brain and the spinal cord. The spinal cord assists the overall communication network of the human anatomy through the brain. The mobility of body and the structure of the whole skeleton is also balanced with the help of the spinal bone, along with reflex control. According to the Global Burden of Disease 2010, worldwide, back pain issues are the leading cause of disability. The clinical specialists in the field estimate almost 80% of the population with experience of back issues. The segmentation of the vertebrae is considered a difficult procedure through imaging. The problem has been catered by different researchers using diverse hand-crafted features like Harris corner, template matching, active shape models, and Hough transform. Existing methods do not handle the illumination changes and shape-based variations. The low-contrast and unclear view of the vertebrae also makes it difficult to get good results. In recent times, convolutional nnural Network (CNN) has taken the research to the next level, producing high-accuracy results. Different architectures of CNN such as UNet, FCN, and ResNet have been used for segmentation and deformity analysis. The aim of this review article is to give a comprehensive overview of how different authors in different times have addressed these issues and proposed different mythologies for the localization and analysis of curvature deformity of the vertebrae in the spinal cord.

scholarly journals Cannabidiol induces autophagy via ERK1/2 activation in neural cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Talita A. M. Vrechi ◽  
Anderson H. F. F. Leão ◽  
Ingrid B. M. Morais ◽  
Vanessa C. Abílio ◽  
Antonio W. Zuardi ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Neurodegenerative Disorders ◽  
Molecular Mechanisms ◽  
Cannabis Sativa ◽  
Autophagic Flux ◽  
Neural Cells ◽  
Human Neuroblastoma ◽  
Trpv1 Receptor ◽  
The Central Nervous System ◽  
Catabolic Process

AbstractAutophagy is a lysosomal catabolic process essential to cell homeostasis and is related to the neuroprotection of the central nervous system. Cannabidiol (CBD) is a non-psychotropic phytocannabinoid present in Cannabis sativa. Many therapeutic actions have been linked to this compound, including autophagy activation. However, the precise underlying molecular mechanisms remain unclear, and the downstream functional significance of these actions has yet to be determined. Here, we investigated CBD-evoked effects on autophagy in human neuroblastoma SH-SY5Y and murine astrocyte cell lines. We found that CBD-induced autophagy was substantially reduced in the presence of CB1, CB2 and TRPV1 receptor antagonists, AM 251, AM 630 and capsazepine, respectively. This result strongly indicates that the activation of these receptors mediates the autophagic flux. Additionally, we demonstrated that CBD activates autophagy through ERK1/2 activation and AKT suppression. Interestingly, CBD-mediated autophagy activation is dependent on the autophagy initiator ULK1, but mTORC1 independent. Thus, it is plausible that a non-canonical pathway is involved. Our findings collectively provide evidence that CBD stimulates autophagy signal transduction via crosstalk between the ERK1/2 and AKT kinases, which represent putative regulators of cell proliferation and survival. Furthermore, our study sheds light on potential therapeutic cannabinoid targets that could be developed for treating neurodegenerative disorders.

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