Abstract
Chronic inflammation is characterized by longstanding microglial activation followed by sustained release of inflammatory mediators, which aid in enhanced nitrosative and oxidative stress. The sustained release of inflammatory mediators propels the inflammatory cycle by increased microglial activation, promoting their proliferation and thus stimulating enhanced release of inflammatory factors. Elevated levels of several cytokines and chronic neuroinflammation have been associated with many neurodegenerative disorders of central nervous system like age-related macular degeneration, Alzheimer disease, multiple sclerosis, Parkinson’s disease, Huntington’ disease, and tauopathies. This review highlights the basic mechanisms of neuroinflammation, the characteristics of neurodegenerative diseases, and the main immunologic responses in CNS neurodegenerative disorders. A comprehensive outline for the crucial role of microglia in neuroinflammation and neurodegeneration and the role of Toll-like receptor signalling in coexistence of inflammatory mechanisms and oxidative stress as major factors responsible for progression of neurodegeneration have also been presented.
Keywords: Microglia, neurodegenerative disorders, neuroinflammation, oxidative stress, toll-like receptors.
CNS & Neurological Disorders - Drug Targets
Title:Inflammatory Mechanisms and Oxidative Stress as Key Factors Responsible for Progression of Neurodegeneration: Role of Brain Innate Immune System
Volume: 15 Issue: 3
Author(s): Jerzy Leszek, George E. Barreto, Kazimierz Gąsiorowski, Euphrosyni Koutsouraki, Marco Ávila-Rodrigues and Gjumrakch Aliev
Affiliation:
Keywords: Microglia, neurodegenerative disorders, neuroinflammation, oxidative stress, toll-like receptors.
Abstract: Chronic inflammation is characterized by longstanding microglial activation followed by sustained release of inflammatory mediators, which aid in enhanced nitrosative and oxidative stress. The sustained release of inflammatory mediators propels the inflammatory cycle by increased microglial activation, promoting their proliferation and thus stimulating enhanced release of inflammatory factors. Elevated levels of several cytokines and chronic neuroinflammation have been associated with many neurodegenerative disorders of central nervous system like age-related macular degeneration, Alzheimer disease, multiple sclerosis, Parkinson’s disease, Huntington’ disease, and tauopathies. This review highlights the basic mechanisms of neuroinflammation, the characteristics of neurodegenerative diseases, and the main immunologic responses in CNS neurodegenerative disorders. A comprehensive outline for the crucial role of microglia in neuroinflammation and neurodegeneration and the role of Toll-like receptor signalling in coexistence of inflammatory mechanisms and oxidative stress as major factors responsible for progression of neurodegeneration have also been presented.
Export Options
About this article
Cite this article as:
Leszek Jerzy, Barreto E. George, Gąsiorowski Kazimierz, Koutsouraki Euphrosyni, Ávila-Rodrigues Marco and Aliev Gjumrakch, Inflammatory Mechanisms and Oxidative Stress as Key Factors Responsible for Progression of Neurodegeneration: Role of Brain Innate Immune System, CNS & Neurological Disorders - Drug Targets 2016; 15 (3) . https://dx.doi.org/10.2174/1871527315666160202125914
DOI https://dx.doi.org/10.2174/1871527315666160202125914 |
Print ISSN 1871-5273 |
Publisher Name Bentham Science Publisher |
Online ISSN 1996-3181 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
Related Articles
-
Fibrosis as a Therapeutic Target Post-Myocardial Infarction
Current Pharmaceutical Design Circulating Biomarkers Determining Inflammation in Atherosclerosis Progression
Current Medicinal Chemistry Therapeutic Angiogenesis for Islet Revascularization
Immunology, Endocrine & Metabolic Agents in Medicinal Chemistry (Discontinued) Novel Inflammatory Biomarkers in Cardiovascular Therapeutics
Current Medicinal Chemistry Simvastatin and Other HMG-CoA Reductase Inhibitors on Brain Cholesterol Levels in Alzheimers Disease
Current Alzheimer Research Mitochondrial Therapeutics for Cardioprotection
Current Pharmaceutical Design Is Nitric Oxide Assuming a Janus-Face in The Central Nervous System?
Current Medicinal Chemistry Update on AKI Biomarker Patents
Current Biomarkers (Discontinued) Cell Therapy for the Treatment of Chronic Ischemic Heart Disease
Current Pharmaceutical Design Recent Patents on Oxidative Stress-Related Biomarkers in Chronic Heart Failure: The Central Role of Endothelium and Myeloperoxidase
Recent Patents on Biomarkers Design and Synthesis of an Aniline Derivative with Biological Activity on Heart Failure
Combinatorial Chemistry & High Throughput Screening Glucagon and Glucagon-Like Peptide Receptors as Drug Targets
Current Pharmaceutical Design Leukotriene A4 Hydrolase as a Target for Cancer Prevention and Therapy
Current Cancer Drug Targets A Comprehensive Review of the Genus Pyrola Herbs in Traditional Uses, Phytochemistry and Pharmacological Activities
Current Topics in Medicinal Chemistry The Importance of Novel Inflammatory Biomarkers in Renal Disease
Current Medicinal Chemistry The Role of the Endothelium in the Pathogenesis of Atherosclerosis and its Therapeutic Implications
Immunology, Endocrine & Metabolic Agents in Medicinal Chemistry (Discontinued) Human Urotensin II Promotes Hypertension and Atherosclerotic Cardiovascular Diseases
Current Medicinal Chemistry MICA Molecules in Disease and Transplantation, a Double-Edged Sword?
Current Immunology Reviews (Discontinued) Cyclooxygenase-2 Inhibitors: A Painful Lesson
Cardiovascular & Hematological Disorders-Drug Targets Discovery and Development of GSK3 Inhibitors for the Treatment of Type 2 Diabetes
Current Pharmaceutical Design