Neuron Glia Interaction in Neuroinflammation

In this book, we focused on neuron-glia interaction of various aspects for understanding of pathophysiology of neuroinflammation in development of inflammatory as well as degenerative neurological disorders.

Neuron Glia Interaction in Neuroinflammation

Accumulation on glia is an active pathological element in many neurological disorders. Gliosis produces neuroinflammation through both neurotrophic and inflammatory means, but the exact mechanism through which this happens remain unclear. It is suspected that damage to neurons activates the growth of glial cells. The proposed book focuses on the interaction between neurons and glia to help elucidate the pathophysiology of neuroinflammation in neurological disorders.​

Interaction Between Neurons and Glia in Aging and Disease

A superb source of reference reviews as well as a concise overview of the functional cross-talk between neurons and glial cells, this book also focuses on microglia and inflammation in the aging brain and in neurological disorders.

Interaction Between Neurons and Glia in Aging and Disease

A superb source of reference reviews as well as a concise overview of the functional cross-talk between neurons and glial cells, this book also focuses on microglia and inflammation in the aging brain and in neurological disorders. The scientific spectrum covered by this book is of key interest, and is recognized by the scientific community as a major competitive area with critical implications for human health.

Neuroinflammation in Neuronal Death and Repair

Tripartite synapses: Glia, the unacknowledged partner. ... Synaptic activation of glutamate transporters in hippocampal astrocytes. Neuron ... Microdomains for neuron-glia interaction: Parallel fiber signaling to Bergmann glial cells.

Neuroinflammation in Neuronal Death and Repair

A current review of the mechanisms of neuroinflammation and their role in neurodegenerative disorders.

The Perioperative Neurocognitive Disorders

Hippocampus CA1 neuron Microglial cell Consequences of neuroinflammation Synaptic dysfunction Neuronal death ... 9.1 Neuroinflammation following surgery-induced neurocognitive impairment via neuron-glia functional mal-interaction.

The Perioperative Neurocognitive Disorders

A practical guide to perioperative cognitive disorders, the most common complications of anesthesia and surgery in older people.

Purinergic Signalling in Neuron Glia Interactions

The well-being of neurons and their functional properties are dependent on glial cells. ... However, it is now appreciated that neuroinflammation is a common pathway and, if we wish to understand how CNS function is impaired, ...

Purinergic Signalling in Neuron Glia Interactions

ATP, the intracellular energy source, is also an extremely important cell–cell signalling molecule for a wide variety of cells across evolutionarily diverse organisms. The extracellular biochemistry of ATP and its derivatives is complex, and the multiple membrane receptors that it activates are linked to many intracellular signalling systems. Purinergic signalling affects a diverse range of cellular phenomena, including ion channel function, cytoskeletal dynamics, gene expression, secretion, cell proliferation, differentiation and cell death. Recently, this class of signalling molecules and receptors has been found to mediate communication between neurons and non-neuronal cells (glia) in the central and peripheral nervous systems. Glia are critical for normal brain function, development and response to injury. Neural impulse activity is detected by glia and purinergic signalling is emerging as a major means of integrating functional activity between neurons, glia and vascular cells in the nervous system. These interactions mediate effects of neural activity on the development of the nervous system and in association with injury, neurodegeneration, myelination and cancer. Bringing together contributions from experts in diverse fields, including glial biologists, neurobiologists and specialists in purinergic receptor structure and pharmacology, this book considers how extracellular ATP acts to integrate communication between different types of glia, and between neurons and glia. Beginning with an overview of glia and purinergic signalling, it contains detailed coverage of purine release, receptors and reagents, purinergic signalling in the neural control of glial development, glial involvement in information processing, and discussion of the interactions between neurons and microglia.

Neuro Immune Interactions in Inflammation and Autoimmunity

It has been suggested that neuroinflammation may not just be the result of the cell loss seen in Parkinson's disease, but that noradrenergic and cholinergic hypofunction may contribute to dysregulation of neuron-glia interactions, ...

Neuro Immune Interactions in Inflammation and Autoimmunity

The nervous system plays an important role in the regulation of immunity and inflammation. On the other hand unbalanced immune responses in inflammatory and autoimmune conditions may have a deleterious impact on neuronal integrity and brain function. Recent studies have characterized neural pathways communicating peripheral inflammatory signals to the CNS, and brain- and spinal cord-derived circuitries controlling various innate and adaptive immune responses and inflammation. A prototypical neural reflex circuit that regulates immunity and inflammation is the vagus nerve-based “inflammatory reflex”. Ongoing research has revealed cellular and molecular mechanisms underlying these neural circuits and indicated new therapeutic approaches in inflammatory and autoimmune disorders. Pharmacological and bioelectronic modulation of neural circuitry has been successfully explored in preclinical settings of sepsis, arthritis, inflammatory bowel disease, obesity-driven disorders, diabetes and other diseases. These studies paved the way to successful clinical trials with bioelectronic neuronal modulation in rheumatoid arthritis and inflammatory bowel disease. Dysregulated release of cytokines and other inflammatory molecules may have a severe impact on brain function. Brain inflammation (neuroinflammation), imbalances in brain neuronal integrity and neurotransmitter systems, and cognitive impairment are characteristic features of post-operative conditions, sepsis, liver diseases, diabetes and other disorders characterized by immune and metabolic dysregulation. Derangements in cytokine release also play a pivotal role in depression. Characteristic brain reactive antibodies in autoimmune conditions, including systemic lupus erythematosus and neuromyelitis optica, significantly contribute to brain pathology and cognitive impairment. These studies, and the simultaneous characterization of neuro-protective cytokines, identified new therapeutic approaches for treating neurological complications in inflammatory and autoimmune disorders. This Frontiers Research Topic is a forum for publishing research findings and methodological and conceptual advances at the intersection of immunology and neuroscience. We hope that presenting new insight into bi-directional neuro-immune communication in inflammation and autoimmunity will foster further collaborations and facilitate the development of new efficient therapeutic strategies.

Neuroinflammation From Bench to Bedside

The ensuing abutment of microglial and neuronal cell bodies provides a spatial arrangement that allows for a number of neuron - glia interactions to occur . Perineuronal microglia displace synaptic terminals ( Blinzinger and Kreutzberg ...

Neuroinflammation     From Bench to Bedside

This book deals with the subject of neuroinflammation and attempts to take the reader on a journey from the bench to the bedside. The microglia and their response to brain injury as well as the importance of the chemokine family are discussed. The relevance of neuroinflammation in experimental models of BSE, scrapie and vCJD as well as Alzheimer's disease, stroke and multiple sclerosis is investigated before proceeding to clinical aspects of neuroinflammation and its involvement in human disease pathophysiology. The book provides an excellent introduction to the field of neuroinflammation and its involvement in human neurodegenerative disease.

Spinal Cord Injury Pain

Neuron-glia interactions after nerve lesion promote and maintain CNP .......................................................................... Inflammatory molecules of secondary lesion cascades are involved in cell communication ...

Spinal Cord Injury Pain

Spinal Cord Injury Pain presents the basis for preclinical and clinical investigations, along with strategies for new approaches in the treatment of central neuropathic pain. Contributors from the private sector and academia provide a comprehensive review of state-of-the-art research in this challenging space. Topics include Epidemiology of Chronic Pain Following SCI, experimental models and mechanisms of chronic pain in SCI, and new targets and technologies. This book serves as a resource for continued translational research that will result in novel approaches and treatments that improve function and quality of life for individuals with CNP/SCI. Despite a better understanding of the complexity of mechanisms of CNP/SCI, improved medical and surgical management of SCI, and the subsequent acceleration of the identification of new targets and the development of novel analgesics, there is still a great unmet clinical need in the area of CNP following SCI. Hence, this book is a welcomed addition to current research and developments. Provides a comprehensive resource for novel approaches and treatments that improve function and quality of life for individuals with CNP/SCI Includes contributors from the private sector and academia Covers epidemiology of chronic pain following SCI, experimental models, mechanisms of chronic pain in SCI, and new targets and technologies

Neuroinflammation

These findings are consistent with numerous studies demonstrating that certain neuronglia interactions can lead to neuronal death [103–108]. Importantly, the PD risk-lowering effects ...

Neuroinflammation

Inflammation is a central mechanism in many neurological diseases, including stroke, multiple sclerosis, and brain trauma as well as meningitis and contributes to the generation of pain. We are now beginning to understand the impact of the immune system on different nervous system functions and diseases, ranging from damage through tolerance to modulation and repair. This book discusses some of the more common neuro-inflammatory diseases. Topics covered include multiple sclerosis, optic neuritis and Susac syndrome. Comprehensive review of the latest developments in neuroinflammation Includes contributions from leading authorities

Neuroinflammation

Schlomann, U., Rathke-Hartlieb, S., Yamamoto, S., Jockusch, H., and Bartsch, J. W. (2000) Tumor necrosis factor a induces a metalloprotease-disintegrin, ADAM8 (CD 156): implications for neuron-glia interactions during neurodegeneration.

Neuroinflammation

In this thoroughly updated and revised edition of his much praised book, Paul L. Wood and a panel of leading researchers capture these new developments in a masterful synthesis of what is known today about the inflammatory mediators and cells involved in neurodegenerative diseases. This second edition contains extensive updates on the mediators produced by microglia and their role in neuroinflammatory-induced neuronal lysis. There is also increased coverage of the animal models used in the study of neuroinflammatory mechanisms, of the new imaging methods that allow the noninvasive evaluation of microglial activation in human neurodegernerative disorders, and of the role of neuroinflammation in amyloid-dependent neuronal lysis.

Modulating Glial Cells Phenotype New Findings and Therapies

Glia-neuron crosstalk in neuroinflammation, neurodegeneration and neuroprotection. Brain Res. ... Glucocorticoid receptor-nitric oxide crosstalk and vulnerability to experimental Parkinsonism: pivotal role for glia-neuron interactions.

Modulating Glial Cells Phenotype  New Findings and Therapies


Neurorepair Strategies to Induce Angiogenesis Neurogenesis and Synaptic Plasticity

Clinical PET imaging of microglial activation: implications for microglial therapeutics in alzheimer's disease. Front. Aging Neurosci. ... Neuron-microglia interaction in neuroinflammation. Curr. Protein Pept. Sci.

Neurorepair Strategies to Induce Angiogenesis  Neurogenesis and Synaptic Plasticity


Neuroinflammation and CNS Disorders

The first section of the book highlights the basic concepts in the field whilst the second section, the main body of the book, covers the role of the immune response in specific disorders of the central nervous system.

Neuroinflammation and CNS Disorders

The last decade has seen an upsurge of information on the role of immune responses in neurodegenerative disorders. In many of these diseases it is still unclear whether the innate and adaptive responses are pathogenic or play a role in repair, and thus understanding their precise roles is key to controlling these diseases by designing immune-therapeutic approaches. The connection between many neurological diseases is the realisation that the immune and nervous systems are inextricable linked, and that perturbations in this delicate balance are involved in many disorders. This has opened up new avenues for therapeutic approaches to treatment of CNS inflammatory and neurodegenerative disorders. Neuroinflammation and CNS Disorders brings together the very latest information on the interactions between the immune system and central nervous system. The first section of the book highlights the basic concepts in the field whilst the second section, the main body of the book, covers the role of the immune response in specific disorders of the central nervous system. Neuroinflammation and CNS Disorders will provide an invaluable guide for both researchers and clinicians working in this complex and dynamic field.

The Role of Apolipoprotein E in Regulating Tau Pathogenesis and Neurodegeneration in a Tauopathy Mouse Model

APOE4 is the strongest genetic risk factor for late-onset Alzheimer's disease (AD).

The Role of Apolipoprotein E in Regulating Tau Pathogenesis and Neurodegeneration in a Tauopathy Mouse Model

APOE4 is the strongest genetic risk factor for late-onset Alzheimer's disease (AD). APOE4 increases brain amyloid-[beta] (A[beta]) pathology relative to other APOE isoforms. However, whether APOE independently influences tau pathology, the other pathological hallmark of AD and other tauopathies, or tau-mediated neurodegeneration, is not clear. By generating P301S tau transgenic mice on either a human APOE knock in (KI) or APOE knockout (KO) background, we show that the presence of human APOE, regardless of APOE isoforms, leads to various degrees of brain atrophy in 9-month old P301S mice, whereas APOE ablation strongly protects against neurodegeneration. In particular, P301S/E4 mice develop significantly more brain atrophy compared with P301S/E2 and P301S/E3 mice. Concomitantly, APOE-sufficient P301S mice develop ptau staining patterns distinct from P301S/EKO mice, with P301S/E4 mice displaying a yet another different pattern from P301S/E2 and P301S/E3 mice that indicates severe neurodegeneration. In diseased P301S mouse brain, APOE specifically binds to a high-molecular-weight tau species and may affect tau pathogenesis through direct APOE-tau interaction. APOE level strongly correlates with ptau levels, and is associated with less soluble tau and more insoluble tau. In addition to affecting tau pathology and neurodegeneration, APOE has potent immunomodulatory functions. In vitro, E4-expressing microglia produce more proinflammatory cytokines following LPS treatment compared with E2- and E3-expressing microglia. In vivo, P301S/E4 mice show markedly enhanced neuroinflammation compared to P301S/E2 and P301S/E3 mice, whereas P301S/EKO mice are largely protected from the change. Co-culturing P301S tau-expressing neurons with mixed glia (80-90% astrocytes + 10-20% microglia) derived from human APOE KI and APOE KO mice results in a marked neuronal loss in the neuron/E4 co-culture with a concomitant elevation of TNF[alpha] level in the medium compared to neuron/E2 and neuron/E3 co-cultures, whereas neurons co-cultured with EKO glia exhibit the greatest viability with the lowest level of secreted TNF[alpha]. In contrast, treatment of P301S neurons with recombinant APOE (E2, E3, E4) in the absence of glial cells only leads to a mild neuronal impairment compared to the absence of APOE, indicating that APOE regulates neurodegeneration in part through glia-mediated neuroinflammation. The effect of APOE on glia-mediated neuronal loss requires direct contact between neurons and glia cells, and APOE may serve as an opsonin bridging stressed neurons that present 'eat-me' signals on cell surfaces with microglia by binding to triggering receptor expressed on myeloid cells 2 (TREM2) to promote neuronal phagoptosis by microglia. APOE is also required for microglial polarization into a neurodegenerative phenotype characterized by a proinflammatory profile and enhanced phagocytotic activity. Depleting microglia from mouse brain using the colony-stimulating factor 1 receptor (CSF1R) inhibitor - PLX3397, rescues neurodegeneration in TE4 mice, but shows no impact on TEKO mice, indicating critical roles of microglia in neurodegeneration regulated by APOE. Reducing APOE levels in P301S mice by overexpressing an APOE receptor, the low-density lipoprotein receptor (LDLR), significantly attenuates neurodegeneration and shifts the ptau staining towards an early-disease pattern. In addition, LDLR overexpression leads to a significant reduction of ptau levels, similar to that observed in P301S /EKO mice.

Recent Advances in Parkinson s Disease

Signaling pathways regulating neuron-glia interaction and their implications in Alzheimer's disease. ... MPTPinduced neuroinflammation increases the expression of pro-inflammatory cytokines and their receptors in mouse brain.

Recent Advances in Parkinson s Disease

Recent Advances in Parkinson ́s Disease Research, Volume 252, represents a follow-up on two previous volumes presented in the Progress in Brain Research series, Volumes 193 and 193, both published in 2010. It contains a collection of overview articles written by leading researchers in Parkinson's, discussing the most important advances made in basic, translational and clinical research. Topics of note in this new release include What can we learn from iPS cell models of PD, What can we learn from animal models of PD?, Molecular basis of selective neuronal vulnerability in PD, Role of innate and adaptive immunity in Parkinson ́s disease, and much more. Covers all key aspects of current research on Parkinson ́s disease Includes topics that range from basic studies on disease models and pathogenic pathways (e.g., protein misfolding, immune and glial mechanisms) to clinical studies on disease features, microbiome, pathophysiology and therapeutic approaches Presents articles authored by world leaders in their respective fields

Adenosine Receptors in Neurodegenerative Diseases

... signals with neurons and influences synaptic activity in healthy brains suggested that alterations of neuron-glia ... and neuroinflammation, since in these mechanisms the intercellular interaction between neurons and glia is ...

Adenosine Receptors in Neurodegenerative Diseases

Adenosine Receptors in Neurodegenerative Diseases covers the role of adenosine receptors in brain function, also focusing on related methodologies and perspectives in therapeutics. The book provides an up-to-date overview by the best specialists in the field, helping readers consider the importance of adenosine and expand the global impact and visibility of adenosine research in the CNS field. Chapters include adenosine biology and signaling, gene regulation, control of motor function, and novel adenosine-based therapies in the CNS. It is an ideal resource for researchers, advanced graduate students, clinicians, and industry scientists working in the fields of clinical neuroscience and molecular and cellular neuroscience. Comprehensive reference that details adenosine receptors in neurodegenerative disorders, with details on brain function and possible therapeutics Gives insights on how these receptors modulate the neurodegenerative outcomes in different disorders Edited by two of the leading researchers in the field regarding adenosine role in the brain in aging and neurodegenerative conditions

Estrogens and Memory

Ramesh G, MacLean AG, Philipp MT (2013) Cytokines and chemokines at the crossroads of neuroinflammation, ... Ricci G, Volpi L, Pasquali L, Petrozzi L, Siciliano G (2009) Astrocyte-neuron interactions in neurological disorders.

Estrogens and Memory

"A book about the influence of estrogens on memory would have been unthinkable as recently as 30 years ago. Although a few small studies in the late 1970's reported a beneficial effect of estrogens on memory in human women (Hackman and Galbraith, 1976; Fedor-Freybergh, 1977), examination of the role of estrogens in memory did not truly capture more widespread attention until the pioneering work of Barbara Sherwin and colleagues in 1988 and beyond. In her initial paper, Sherwin showed that bilateral removal of the ovaries (aka surgical menopause) led to impaired short-term and long-term memory, whereas treatment of surgically menopausal women with estradiol alone, testosterone alone, or estradiol plus testosterone prevented this decline (Sherwin, 1988). As a search for the terms "estrogen" and "memory" in PubMed illustrates, well over 2000 papers have been published on the subject of estrogens and memory in the ensuing decades. The vast majority of these studies have focused on the hippocampus, a bilateral medial temporal lobe structure essential for the formation of episodic memories, particularly those with spatial, contextual, relational, temporal, and recognition components (Olton et al., 1979; Morris et al., 1982; Kim and Fanselow, 1992; Squire, 1992; Cohen and Stackman, 2015; Tonegawa et al., 2015; Eichenbaum, 2017). Although various forms of learning and memory are mediated by numerous brain regions, including the prefrontal cortex, medial temporal lobe cortices, amygdala, striatum, and cerebellum, the hippocampus has received the lion's share of attention due to its central importance for episodic memory formation. Hippocampal damage produces profound retrograde amnesia for facts and events, as well as anterograde amnesia for new information and impairments in spatial navigation (Winocur, 1990; Anagnostaras et al., 2001; Clark et al., 2002; Gilboa et al., 2006). Hippocampal dysfunction in middle-aged and aged subjects is a primary contributor to age-related memory decline (Golumb et al., 1996; Grady et al., 2003; Apostolova et al., 2010; Burke and Barnes, 2010; Small et al., 2011; Yassa et al., 2011), and has also been implicated in the cognitive impairments observed in diseases such as schizophrenia and depression (Small et al., 2011; Nakahara et al., 2018; Santos et al., 2018; Ott et al., 2019). Moreover, the hippocampi of patients with Alzheimer's disease are substantially atrophied and burdened with copious amounts of amyloid plaques and neurofibrillary tangles, the hallmark pathologies of this insidious disease (Hyman et al., 1984; Walsh and Selkoe, 2004; Selkoe and Hardy, 2016). As such, understanding how estrogens influence hippocampal functioning may provide important insights not only about the fundamental neurobiology of memory processes, but also into the etiology of neuropsychiatric and neurodegenerative diseases"--

The Alzheimer s Disease Challenge

... modulates production of neurotransmitters and molecules with neurotrophic activity, prevents apoptosis, suppresses neuroinflammation, affects neuron-glia interactions, thereby enhancing cognition, learning, and social communications ...

The Alzheimer s Disease Challenge

Alzheimer’s disease is undoubtedly the major health challenge of our Century with significant social and economic consequences. This Frontiers eBook offers a contribution of 39 innovative papers on the multidimensional and crucial problem of Alzheimer’s disease management and treatment. Several perspectives, research updates, and trials describing methods on potential diagnosis and treatment are presented including biological mechanisms, biomarkers and risk factors for an early and efficient prognosis, diagnosis and prevention. Additionally, while the rapidly increasing Alzheimer’s disease population demands holistic solutions and clinical studies with new therapeutic target approaches, several of the contributive papers present promising drugs targeting Alzheimer’s disease treatment. We give our deepest acknowledgment to all the authors for their important and innovative contributions, to the reviewers for their valuable recommendations on improving the submitting studies and all the Frontiers Editorial team for continuous support.

Monitoring endogenous GPCRs lessons for drug design

... this model was used to investigate microglia proliferation during early embryonic spinal cord invasion (Rigato et al., 2012) neuron-glia interactions in the context of nerve injury or neuroinflammation (Garcia etal., ...

Monitoring endogenous GPCRs  lessons for drug design

G protein-coupled receptors (GPCRs) are integral membrane proteins forming the fourth largest superfamily in the human genome. Many of these receptors play key physiological roles and several pathologies have been associated with receptor functional abnormalities. GPCRs therefore represent important goals for drug design in pharmaceutical companies since they constitute the target of about one third of the drugs currently on the market. However, endogenous GPCRs are most often difficult to study because of a lack of tools to target them specifically and single out their response to physiological or drug-elicited stimulations. Hence, studies mostly focused on recombinant receptors expressed in a variety of cellular models that do not always closely reflect the receptor natural environment and often deal with levels of expression exceeding by far physiological ranges. Recent technological developments combining for example genetically modified animals and advanced imaging approaches have improved our ability to visualize endogenous GPCRs. To date, trailing receptor activation, subsequent intracellular redistribution, changes in signaling cascade up to integrated response to a drug-elicited stimulation is at hand though the impact of a physiological challenge on receptor dynamics remains a major issue. Data however suggest that the receptor may embrace a different fate depending on the type of stimulation in particular if sustained or repeated. This suggests that current drugs may only partially mimic the genuine response of the receptor and may explain, at least in part, their secondary effects. Commonalities and specificities between physiological and drug-induced activation can thus represent valuable guidelines for the design of future drugs.

Molecular Basis of Neuropsychiatric Disorders from Bench to Bedside

Moreover, several studies suggest that systemic administration of LPS contributes to glial activation and ... of the interplay between microglial activation, neuroinflammation and neuron-glia interactions in the MDDrelevant brain ...

Molecular Basis of Neuropsychiatric Disorders  from Bench to Bedside

Progress in Molecular Biology and Translational Science, Volume 167, provides the most topical, informative and exciting monographs available on a wide variety of research topics related to Models and Biological Targets in Drug Discovery for Attention Deficit Hyperactivity Disorder, Novel Targets for Parkinson-Depression Co-morbidity. Utility of Cannabidiol (CBD) in Neuropsychiatric Disorders: A Short Review of the Recent Pre-clinical and Clinical Findings, The Many Sides of Microglia in Alcohol Use Disorders, Stress, Anxiety, Molecular Targets and More, Calcineurin Signaling in Psychiatric Disorders, Emerging Evidence for the Role of Pituitary Adenylate Cyclase- Activating Peptide (PACAP) in Neuropsychiatric Disorders, and more. Includes comprehensive coverage of molecular biology Presents ample use of tables, diagrams, schemata and color figures to enhance the reader's ability to rapidly grasp the information provided Contains contributions from renowned experts in the field