scholarly journals Role of hydrogen sulfide and polysulfides in neurological diseases: focus on protein S-Persulfidation

2020 ◽  
Vol 18 ◽  
Author(s):  
Hai-Jian Sun ◽  
Zhi-Yuan Wu ◽  
Xiao-Wei Nie ◽  
Jin-Song Bian
Keyword(s):  
Hydrogen Sulfide ◽  
Protein Modification ◽  
Neurological Diseases ◽  
Protein S ◽  
The Body ◽  
Memory Decline ◽  
Target Proteins ◽  
Therapeutic Development ◽  
The Central Nervous System

: Hydrogen sulfide (H2S) and hydrogen polysulfides are recognized as important signaling molecules that are generated physiologically in the body, including the central nervous system (CNS). Studies have shown that these two molecules are involved in cytoprotection against oxidative stress and inflammatory response. In the brain system, H2S and polysulfides exert multiple functions in both health and diseases, including Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington's disease (HD), memory decline, and glioma. Mechanistically, S-Persulfidation (also known as S-sulfuration or S-sulfhydration) of target proteins is believed to be a fundamental mechanism that underlies H2S-regulated signaling pathways. Cysteine S-Persulfidation is an important paradigm of post-translational protein modification in the process of H2S signaling. This model is established as a critical redox mechanism to regulate numerous biological functions, especially in H2S-mediated neuroprotection and neurogenesis. Although the current research of S-Persulfidation is still in its infancy, accumulative evidence suggests that protein S-Persulfidation may share similar characteristics with protein S-nitrosylation. In this review, we will provide a comprehensive insight into the S-Persulfidation biology of H2S and polysulfides in neurological ailments and presume potential avenues for therapeutic development in these disorders based on S-Persulfidation of target proteins.

scholarly journals Src Family Kinases in the Central Nervous System：Their Emerging Role in Pathophysiology of Migraine and Neuropathic Pain

2020 ◽  
Vol 18 ◽  
Author(s):  
Lingdi Nie ◽  
Wen-Rui Ye ◽  
Shangbin Chen ◽  
Domenico Chirchiglia ◽  
Minyan Wang
Keyword(s):  
Neuropathic Pain ◽  
Tyrosine Kinases ◽  
Neurological Diseases ◽  
Src Family Kinases ◽  
Signalling Pathways ◽  
Pain Mechanisms ◽  
Promising Therapeutic Target ◽  
The Central Nervous System ◽  
The Relationship

: Src family kinases (SFK) are a group of non-receptor tyrosine kinases which play a pivotal role in cellular responses and oncogenesis. Accumulating evidence suggest that SFK also act as a key component in signalling pathways of the central nervous system (CNS) in both physiological and pathological conditions. Despite the crucial role of SFK in signal transduction of the CNS, the relationship between SFK and molecules implicated in pain has been relatively unexplored. This article briefly reviews the recent advances uncovering the interplay of SFK with diverse membrane proteins and intracellular proteins in the CNS and the importance of SFK in the pathophysiology of migraine and neuropathic pain. Mechanisms underlying the role of SFK in these conditions and potential clinical applications of SFK inhibitors in neurological diseases are also summarised. We propose that SFK are the convergent point of signalling pathways in migraine and neuropathic pain and may constitute a promising therapeutic target for these diseases.

scholarly journals Insights Into the Role of CSF1R in the Central Nervous System and Neurological Disorders

2021 ◽  
Vol 13 ◽  
Author(s):  
Banglian Hu ◽  
Shengshun Duan ◽  
Ziwei Wang ◽  
Xin Li ◽  
Yuhang Zhou ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neurological Disorders ◽  
Neurological Diseases ◽  
Colony Stimulating Factor ◽  
Loss Of Function ◽  
Axonal Spheroids ◽  
The Central Nervous System ◽  
Stimulating Factor

The colony-stimulating factor 1 receptor (CSF1R) is a key tyrosine kinase transmembrane receptor modulating microglial homeostasis, neurogenesis, and neuronal survival in the central nervous system (CNS). CSF1R, which can be proteolytically cleaved into a soluble ectodomain and an intracellular protein fragment, supports the survival of myeloid cells upon activation by two ligands, colony stimulating factor 1 and interleukin 34. CSF1R loss-of-function mutations are the major cause of adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP) and its dysfunction has also been implicated in other neurodegenerative disorders including Alzheimer’s disease (AD). Here, we review the physiological functions of CSF1R in the CNS and its pathological effects in neurological disorders including ALSP, AD, frontotemporal dementia and multiple sclerosis. Understanding the pathophysiology of CSF1R is critical for developing targeted therapies for related neurological diseases.

scholarly journals Store-Operated Calcium Channels in Physiological and Pathological States of the Nervous System

2020 ◽  
Vol 14 ◽  
Author(s):  
Isis Zhang ◽  
Huijuan Hu
Keyword(s):  
Nervous System ◽  
Calcium Channels ◽  
Neurological Disorders ◽  
Neurological Diseases ◽  
Physiological Role ◽  
The Body ◽  
Store Operated Calcium Entry ◽  
Important Pathway ◽  
Molecular Components

Store-operated calcium channels (SOCs) are widely expressed in excitatory and non-excitatory cells where they mediate significant store-operated calcium entry (SOCE), an important pathway for calcium signaling throughout the body. While the activity of SOCs has been well studied in non-excitable cells, attention has turned to their role in neurons and glia in recent years. In particular, the role of SOCs in the nervous system has been extensively investigated, with links to their dysregulation found in a wide variety of neurological diseases from Alzheimer’s disease (AD) to pain. In this review, we provide an overview of their molecular components, expression, and physiological role in the nervous system and describe how the dysregulation of those roles could potentially lead to various neurological disorders. Although further studies are still needed to understand how SOCs are activated under physiological conditions and how they are linked to pathological states, growing evidence indicates that SOCs are important players in neurological disorders and could be potential new targets for therapies. While the role of SOCE in the nervous system continues to be multifaceted and controversial, the study of SOCs provides a potentially fruitful avenue into better understanding the nervous system and its pathologies.

scholarly journals Cytomorphological and Cytochemical Identification of Microglia

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Subhajit Das Sarma ◽  
Koushik Chatterjee ◽  
Himadri Dinda ◽  
Dhriti Chatterjee ◽  
Jayasri Das Sarma
Keyword(s):  
Central Nervous System ◽  
Animal Model ◽  
Immune Cells ◽  
Microglial Activation ◽  
Neurological Diseases ◽  
Neuronal Dysfunction ◽  
Ultrastructural Studies ◽  
The Central Nervous System ◽  
Made In

Microglia is one of the major resident immune cells in the central nervous system and is considered to be the key cellular mediator of neuroinflammatory processes. Identification of different Microglial states of activation by morphologic means has been one of the major challenges in the field of neurobiology of diseases. Therefore, microglial biology demands techniques to identify differing stages of microglia in different neuroanatomic locations as well as understanding the role of Microglia in different Neurological diseases. This present study is aimed towards summarizing the literature and for understanding the progress made in different Cytomorphological and Cytochemical techniques of identifying Microglia. This study also review recently used Immunohistochemistry techniques, along with Ultrastructural studies determining different morphological features of resting to activated phagocytic Microglia in a viral induced experimental animal model of neuroinflammation. Results revealed that chronic Microglial activation is considered to be an important component of neuronal dysfunction, injury, and loss (and hence to disease progression). Thus, Microglial research with special emphasis on identification of different activation states of Microglia has gradually become significant.

Role of the glucose-dependent insulinotropic polypeptide and its receptor in the central nervous system: therapeutic potential in neurological diseases

2010 ◽  
Vol 21 (5-6) ◽  
pp. 394-408 ◽  
Author(s):  
Cláudia P. Figueiredo ◽  
Fabrício A. Pamplona ◽  
Tânia L. Mazzuco ◽  
Aderbal S. Aguiar ◽  
Roger Walz ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Therapeutic Potential ◽  
Neurological Diseases ◽  
The Central Nervous System

scholarly journals NGF, Brain and Behavioral Plasticity

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Alessandra Berry ◽  
Erika Bindocci ◽  
Enrico Alleva
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Behavioral Plasticity ◽  
The Body ◽  
Trophic Factor ◽  
Brain Growth ◽  
Male Mice ◽  
Psychosocial Stressor ◽  
The Central Nervous System

Nerve Growth Factor (NGF) was initially studied for its role as a key player in the regulation of peripheral innervations. However, the successive finding of its release in the bloodstream of male mice following aggressive encounters and its presence in the central nervous system led to the hypothesis that variations in brain NGF levels, caused by psychosocial stressor, and the related alterations in emotionality, could be functional to the development of proper strategies to cope with the stressor itself and thus to survive. Years later this vision is still relevant, and the body of evidence on the role of NGF has been strengthened and expanded from trophic factor playing a role in brain growth and differentiation to a much more complex messenger, involved in psychoneuroendocrine plasticity.

scholarly journals Nervous System and Tissue Polarity Dynamically Adapt to New Morphologies in Planaria

2019 ◽  
Author(s):  
Johanna Bischof ◽  
Margot E. Day ◽  
Kelsie A. Miller ◽  
Joshua LaPalme ◽  
Michael Levin
Keyword(s):  
Nervous System ◽  
Planar Cell Polarity ◽  
Tissue Level ◽  
The Body ◽  
Tissue Polarity ◽  
Intact Brain ◽  
Radiation Induced ◽  
The Central Nervous System ◽  
Primary Axis

AbstractThe coordination of tissue-level polarity with organism-level polarity is crucial in development, disease, and regeneration. Exploiting the flexibility of the body plan in regenerating planarians, we used mirror duplication of the primary axis to show how established tissue-level polarity adapts to new organism-level polarity. Tracking of cilia-driven flow to characterize planar cell polarity of the epithelium revealed a remarkable reorientation of tissue polarity in double-headed planarians. This reorientation is driven by signals produced by the intact brain and is not hampered by radiation-induced removal of stem cells. The nervous system itself adapts its polarity to match the new organismal anatomy in these animals as revealed by distinct regenerative outcomes driven by polarized nerve transport. Thus, signals from the central nervous system can dynamically control and re-orient tissue-level polarity to match the organism-level anatomical configuration, illustrating a novel role of the nervous system in the regulation of patterning.

scholarly journals An Update of Palmitoylethanolamide and Luteolin Effects in Preclinical and Clinical Studies of Neuroinflammatory Events

Antioxidants ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 216 ◽  
Author(s):  
Marika Cordaro ◽  
Salvatore Cuzzocrea ◽  
Rosalia Crupi
Keyword(s):  
Nervous System ◽  
Neurological Diseases ◽  
Autism Spectrum ◽  
Monocytes And Macrophages ◽  
Central Nervous Systems ◽  
The Central Nervous System ◽  
Spectrum Disorders ◽  
Dynamic Series ◽  
Preclinical And Clinical Studies

The inflammation process represents of a dynamic series of phenomena that manifest themselves with an intense vascular reaction. Neuroinflammation is a reply from the central nervous system (CNS) and the peripheral nervous system (PNS) to a changed homeostasis. There are two cell systems that mediate this process: the glia of the CNS and the lymphocites, monocytes, and macrophages of the hematopoietic system. In both the peripheral and central nervous systems, neuroinflammation plays an important role in the pathogenesis of neurodegenerative diseases, such as Parkinson’s and Alzheimer’s diseases, and in neuropsychiatric illnesses, such as depression and autism spectrum disorders. The resolution of neuroinflammation is a process that allows for inflamed tissues to return to homeostasis. In this process the important players are represented by lipid mediators. Among the naturally occurring lipid signaling molecules, a prominent role is played by the N-acylethanolamines, namely N-arachidonoylethanolamine and its congener N-palmitoylethanolamine, which is also named palmitoylethanolamide or PEA. PEA possesses a powerful neuroprotective and anti-inflammatory power but has no antioxidant effects per se. For this reason, its co-ultramicronization with the flavonoid luteolin is more efficacious than either molecule alone. Inhibiting or modulating the enzymatic breakdown of PEA represents a complementary therapeutic approach to treating neuroinflammation. The aim of this review is to discuss the role of ultramicronized PEA and co-ultramicronized PEA with luteolin in several neurological diseases using preclinical and clinical approaches.

scholarly journals Eag1 K+Channel: Endogenous Regulation and Functions in Nervous System

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Bo Han ◽  
Tursonjan Tokay ◽  
Guangming Zhang ◽  
Peng Sun ◽  
Shangwei Hou
Keyword(s):  
Nervous System ◽  
Recent Progress ◽  
Neurological Diseases ◽  
Tumor Development ◽  
K Channel ◽  
Oxygen Species ◽  
Voltage Gated ◽  
Channel Regulation ◽  
The Central Nervous System

Ether-à-go-go1 (Eag1, Kv10.1, KCNH1) K+channel is a member of the voltage-gated K+channel family mainly distributed in the central nervous system and cancer cells. Like other types of voltage-gated K+channels, the EAG1 channels are regulated by a variety of endogenous signals including reactive oxygen species, rendering the EAG1 to be in the redox-regulated ion channel family. The role of EAG1 channels in tumor development and its therapeutic significance have been well established. Meanwhile, the importance of hEAG1 channels in the nervous system is now increasingly appreciated. The present review will focus on the recent progress on the channel regulation by endogenous signals and the potential functions of EAG1 channels in normal neuronal signaling as well as neurological diseases.

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