(Ebook PDF) Neuroinflammation in Neuronal Death and Repair 1st Edition by Giacinto Bagetta ISBN 9780080550565 0123739896 full chapters

(Ebook PDF) Neuroinflammation in Neuronal Death and Repair 1st Edition by Giacinto Bagetta -Ebook PDF Instant Download/Delivery:9780080550565, 0123739896

Instant download Full Chapter of  Neuroinflammation in Neuronal Death and Repair 1st Edition  after payment

Product details:

ISBN 10:0123739896

ISBN 13:9780080550565

Author: Giacinto Bagetta

Neuroinflammation has been implicated recently in the pathogenesis of many neurodegenerative diseases. The cross-talk between neurons and non-neuronal cells seems to be a critical step in the progression of neurodegeneration and molecules that have a beneficial role may turn into harmful players. Thus, matrix metalloproteinases (MMPs), which are involved in axonal growth and regeneration as well as synaptic plasticity, may also have detrimental effects. Recent evidence has linked MMPs to conditions like ischemia, multiple sclerosis, Alzheimer’s disease and suggested that, together with their role in the degradation of extracellular macromolecules, MMPs could work as important signalling molecules from injured neurons to the microglia.
Thus, MMP-3 has been shown to induce the release of pro-inflammatory cytokines from microglia via activation of ERK and NF-kB-dependent pathways. Increasing evidence highlights the importance of a balanced cross-talk between neurons and non-neuronal cells and indicates that the presence of reactive astrocytes, the activation of microglia and the release of inflammatory mediators may contribute to the progression of many central nervous system disorders, independently of the nature of the primary pathogenic event. However, many aspects still remain controversial and much more effort is needed to understand the role of neuroinflammatory mediators and processes in these conditions.

Table of Contents:

• Inflammatory Mediators Leading to Protein Misfolding and Uncompetitive/Fast Off–Rate Drug Therapy for Neurodegenerative Disorders
• I Introduction
• II Protein Misfolding in Neurodegenerative Diseases
• III Generation of RNS/ROS
• IV Protein S–Nitrosylation and Neuronal Cell Death
• V Parkin and the UPS
• VI S–Nitrosylation and Parkin
• VII The Unfolded Protein Response and PDI
• VIII S–Nitrosylation of PDI Mediates Protein Misfolding and Neurotoxicity in Cell Models of PD or AD
• IX PDI Activity in ALS and Prion Disease
• X Potential Treatment of Excessive NMDA–Induced Ca2+ Influx and S–Nitrosylation
• XI Looking to the Future: NitroMemantines
• XII Conclusions
• Innate Immunity and Protective Neuroinflammation: New Emphasis on the Role of Neuroimmune Regulatory Proteins
• I Characteristics of the Cellular and Molecular Innate Immune Responses in the Brain
• II Innate Immune Response in Health: The Key Role of Physical Barriers
• III Immunoprivileged Status of the Brain by Preventing the Infiltration of Potentially Harmful Systemic Immune Cells: Roles of ACAMPs
• IV Protective Innate Immune Response During Brain Infection and Inflammation to Promote the Clearance of Pathogens: Roles of PAMPs
• V Interactions of Innate Immune Molecules with Toxic Proteins: Roles of PPAMPs
• VI Regulating the Innate Immune Response in the CNS While Promoting Tissue Repair: Roles of Neuroimmune Regulatory Molecules
• VII Innate Immunity and Neurogenesis
• VIII The Canonical Innate Immune System in the CNS: The Complement System
• IX Conclusion: Elements to Drive Innate Immune Neuroprotective Activities
• Glutamate Release from Astrocytes in Physiological Conditions and in Neurodegenerative Disorders Characterized by Neuroinflammation
• I Introduction
• II Ca2+–Dependent Glutamate Release from Astrocytes
• III Excitotoxicity Involving Ca2+–Dependent Glutamate Release from Astrocytes in Pathological Conditions: The Case of ADC
• IV Astrocytic Alterations and Ca2+–Dependent Glutamate Release Dysfunction in AD
• V Conclusions
• The High–Mobility Group Box 1 Cytokine Induces Transporter–Mediated Release of Glutamate from Glial Subcellular Particles (Gliosomes) Prepared from in Situ–Matured Astrocytes
• I Introduction
• II Gliosomes as a Model to Study Astrocyte Characteristics
• III HMGB1–Induced Glutamate Release from Gliosomes
• IV Concluding Remarks
• The Role of Astrocytes and Complement System in Neural Plasticity
• I Introduction
• II Astrocytes, GFAP, and Astrocyte Intermediate Filaments
• III Reactive Gliosis, Neurotrauma, and CNS Transplants
• IV The Complement System
• New Insights into the Roles of Metalloproteinases in Neurodegeneration and Neuroprotection
• I Introduction
• II The NEP Family
• III The NEP Homologue ECE–1
• IV The ACE Family
• V Ischemia/Hypoxia and Ageing as Factors Affecting Metalloproteinases
• VI Conclusions
• Relevance of High–Mobility Group Protein Box 1 to Neurodegeneration
• I Introduction
• II Structure and Nuclear Functions
• III Cytokine Functions
• IV Role of HMGB1 in CNS (DYS)Function
• V Conclusions
• Early Upregulation of Matrix Metalloproteinases Following Reperfusion Triggers Neuroinflammatory Mediators in Brain Ischemia in Rat
• I Introduction
• II Methods
• III Results
• IV Discussion
• The (Endo)Cannabinoid System in Multiple Sclerosis and Amyotrophic Lateral Sclerosis
• I Introduction
• II The ECS
• III ECS in MS
• IV ECS in ALS
• V Conclusions
• Chemokines and Chemokine Receptors: Multipurpose Players in Neuroinflammation
• I Introduction
• II Fractalkine and Fractalkine Receptor (CX3CR1) Govern Regulatory NK Accumulation and Microglial Activation During Neuroinflammation
• III CXCR2 Regulates Both Monocyte Infiltration and Oligodendrocyte–Mediated Tissue Repair in EAE
• Systemic and Acquired Immune Responses in Alzheimer’s Disease
• I Alzheimer’s Neuropathology
• II Cellular Immune Responses
• III Humoral Immune Responses in the Periphery
• IV Conclusion
• Neuroinflammation in Alzheimer’s Disease and Parkinson’s Disease: Are Microglia Pathogenic in Either Disorder?
• I Introduction
• II Neuroinflammation in AD and PD
• III PD May Provide a More Facile Model for Demonstrating a Pathogenic Role of Neuroinflammation
• IV Advantages of Microglial Cell Cultures
• V Responses of Cultured Microglia to AD and PD Pathology
• VI Conclusions
• Cytokines and Neuronal Ion Channels in Health and Disease
• I Introduction
• II Properties of Ion Channels
• III Distribution and Targeting of Neuronal Ion Channels
• IV Ion Channels Are Targeted by Proinflammatory Cytokines
• V IL–1β and Voltage–Dependent Ca2+ Channels
• VI IL–1β and NMDAR
• VII TNF–α: Few Final Considerations
• VIII Conclusions
• Cyclooxygenase–2, Prostaglandin E2, and Microglial Activation in Prion Diseases
• I Introduction
• II COXs and PGs in Brain Functions
• III Prion Diseases
• IV COXs in Human and Experimental Prion Diseases
• V Roles of COX–2 and PGE2 in Prion Diseases
• Glia Proinflammatory Cytokine Upregulation as a Therapeutic Target for Neurodegenerative Diseases: Function–Based and Target–Based Discovery Approaches
• I Neuroinflammation and Disease Progression
• II CNS Proinflammatory Cytokine Production as a Therapeutic Target for AD
• III De Novo Lead Compound Discovery and the Recent Major Changes in Translational Research at the Chemistry–Biology Interface
• IV Development of Minozac: A Function–Driven Approach to Develop Small Molecule Compounds That Target Proinflammatory Cytokine Upregulation
• Oxidative Stress and the Pathogenesis of Neurodegenerative Disorders
• I Introduction: Free Radicals, Immunity, and the Nervous System
• II Neuropathogenesis of Neurodegeneration
• III Free Radicals and Neurodegenerative Disorders
• IV Glutathione System, Glutamate–Glutamine Cycle, and the CNS
• V Modulators of Microglial Activation
• VI Growth Factors, Antioxidants, and Anti–Inflammatory Drug Therapies
• VII Therapeutic Immunomodulation
• VIII Summary
• Differential Modulation of Type 1 and Type 2 Cannabinoid Receptors along the Neuroimmune Axis
• I Introduction
• II Lipid Rafts and Cannabinoid Receptors
• III Discussion
• Effects of the HIV–1 Viral Protein TAT on Central Neurotransmission: Role of Group I Metabotropic Glutamate Receptors
• I Neurological Complications of HIV–1 Infection
• II The HIV–1 Viral Protein Tat
• III About the Experimental Approach
• IV Effects of Tat on the Release of Neurotransmitters in CNS
• V Effects of Tat on Presynaptic AMPA/Kainate Receptors
• VI Effects of Tat on Presynaptic NMDA Receptors
• VII Effects of Tat on Presynaptic Metabotropic Glutamate Receptors
• VIII Specie Specificity of Tat–Mediated Effects and Amino Acid Sequences Involved
• IX Conclusions
• Evidence to Implicate Early Modulation of Interleukin–1β Expression in the Neuroprotection Afforded by 17β–Estradiol in Male Rats Undergone Transient Middle Cerebral Artery Occlusion
• I Introduction
• II Methods
• III Results
• IV Discussion
• A Role for Brain Cyclooxygenase–2 and Prostaglandin–E2 in Migraine: Effects of Nitroglycerin
• I Introduction
• II Materials and Methods
• III Results
• IV Discussion
• The Blockade of K+–ATP Channels has Neuroprotective Effects in an In Vitro Model of Brain Ischemia
• I Introduction
• II Materials and Methods
• III Results
• IV Discussion
• Retinal Damage Caused by High Intraocular Pressure–Induced Transient Ischemia is Prevented by Coenzyme Q10 in Rat
• I Introduction
• II Materials and Methods
• III Results
• IV Discussion
• Evidence Implicating Matrix Metalloproteinases in the Mechanism Underlying Accumulation of IL–1β and Neuronal Apoptosis in the Neocortex of HIV/gp120–Exposed Rats
• I Introduction
• II Materials and Methods
• III Results
• IV Discussion
• Neuroprotective Effect of Nitroglycerin in a Rodent Model of Ischemic Stroke: Evaluation of Bcl–2 Expression
• I Introduction
• II Materials and Methods
• III Results
• IV Discussion

People also search:

neuroinflammation in neurodegenerative diseases
neuroinflammation in depression
neuronal inflammation
neuroinflammation and neurodegeneration
brain injury inflammation

Tags:

Neuro inflammation,Neuronal Death,Repair,Giacinto Bagetta