Abstract
Although the main cause of many neurodegenerative diseases is unknown, the glial reaction is considered to be a consequence of neuronal cell death in Alzheimers disease, Parkinsons disease, and Huntingtons disease. In Parkinsons disease, postmortem examination and experimental animal models exposed to neurotoxin reveals a dramatic loss of dopaminergic neurons in the substantia nigra associated with a massive astrogliosis and the presence of activated microglial cells. These glial cells can release deleterious compounds such as proinflammatory prostaglandins and cytokines, which may act by stimulating reactive oxygen species in glial cells, or which may exert a more direct effect on dopaminergic neurons by activating receptors that contain death domains involved in neuronal apoptosis. The anti-inflammatory drugs and the tetracycline derivative minocycline have been shown to reduce glial activation and protect the substantia nigra in an animal model of the disease. Inhibition of the glial reaction and the inflammatory processes may thus represent a therapeutic target to reduce neuronal degeneration in Parkinsons disease. Elucidation of molecular mechanisms underlying intracellular signal transductions of glial activation will provide promising means of controlling neuroinflammation and the subsequent neurodegeneration.
Keywords: Neurodegenerative diseases, neuroinflammation, microglia, astrocyte, Parkinson's disease, experimental animal model, minocycline, central nervous system, signal transduction
Current Signal Transduction Therapy
Title: Glial Reaction in Parkinsons Diseases: Inflammatory Activation Signaling of Glia as a Potential Therapeutic Target
Volume: 2 Issue: 1
Author(s): Dong-Kug Choi and Kyoungho Suk
Affiliation:
Keywords: Neurodegenerative diseases, neuroinflammation, microglia, astrocyte, Parkinson's disease, experimental animal model, minocycline, central nervous system, signal transduction
Abstract: Although the main cause of many neurodegenerative diseases is unknown, the glial reaction is considered to be a consequence of neuronal cell death in Alzheimers disease, Parkinsons disease, and Huntingtons disease. In Parkinsons disease, postmortem examination and experimental animal models exposed to neurotoxin reveals a dramatic loss of dopaminergic neurons in the substantia nigra associated with a massive astrogliosis and the presence of activated microglial cells. These glial cells can release deleterious compounds such as proinflammatory prostaglandins and cytokines, which may act by stimulating reactive oxygen species in glial cells, or which may exert a more direct effect on dopaminergic neurons by activating receptors that contain death domains involved in neuronal apoptosis. The anti-inflammatory drugs and the tetracycline derivative minocycline have been shown to reduce glial activation and protect the substantia nigra in an animal model of the disease. Inhibition of the glial reaction and the inflammatory processes may thus represent a therapeutic target to reduce neuronal degeneration in Parkinsons disease. Elucidation of molecular mechanisms underlying intracellular signal transductions of glial activation will provide promising means of controlling neuroinflammation and the subsequent neurodegeneration.
Export Options
About this article
Cite this article as:
Choi Dong-Kug and Suk Kyoungho, Glial Reaction in Parkinsons Diseases: Inflammatory Activation Signaling of Glia as a Potential Therapeutic Target, Current Signal Transduction Therapy 2007; 2 (1) . https://dx.doi.org/10.2174/157436207779317146
DOI https://dx.doi.org/10.2174/157436207779317146 |
Print ISSN 1574-3624 |
Publisher Name Bentham Science Publisher |
Online ISSN 2212-389X |
- 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
- Announcements
Related Articles
-
Cerebrovascular Diseases in HIV-Infected Patients
Current HIV Research The Meaning of Different Forms of Structural Myocardial Injury, Immune Response and Timing of Infarct Necrosis and Cardiac Repair
Current Vascular Pharmacology Central Nervous System Manifestations in Systemic Lupus Erythematosus
Current Rheumatology Reviews Epigenetic Regulation of Myocardial Homeostasis, Self-Regeneration and Senescence
Current Drug Targets The Role of 18FDG PET/CT in the Assessment of Endocarditis, Myocarditis and Pericarditis
Current Radiopharmaceuticals Clinical Characteristics of Behcet’s Disease in 453 Egyptian Patients Suffering from Uveitis with Gender Comparison
Current Rheumatology Reviews Vasopressin Secretion Control: Central Neural Pathways, Neurotransmitters and Effects of Drugs
Current Pharmaceutical Design Cerebral Hypoperfusion During Carotid Artery Stenosis can Lead to Cognitive Deficits that may be Independent of White Matter Lesion Load
Current Neurovascular Research Organizational Impact of the Introduction of a New Portable Syringe Pump for Iloprost Therapy in Italian Hospital Settings
Current Drug Therapy Drugs, Trials and Pathogenesis: Will Connecting these Help us Understand SLE?
Current Rheumatology Reviews Targeting JAK/STAT Signaling Pathway in Inflammatory Diseases
Current Signal Transduction Therapy Transcranial Doppler Ultrasonography: Current Status
Current Medical Imaging Perioperative Considerations in Rheumatoid Arthritis Patients
Current Rheumatology Reviews Pharmacological Pre- and Post- Conditioning Agents: Reperfusion-Injury of the Heart Revisited
Mini-Reviews in Medicinal Chemistry Novel Drug Targets for the Treatment of Cardiac Diseases
Current Pharmacogenomics and Personalized Medicine Sex Steroid Hormones, Cardiovascular Diseases and The Metabolic Syndrome
Cardiovascular & Hematological Agents in Medicinal Chemistry Selective Elevation of Circulating CCL2/MCP1 Levels in Patients with Longstanding Post-vaccinal Macrophagic Myofasciitis and ASIA
Current Medicinal Chemistry New Pharmacological Approaches to the Prevention of Myocardial Ischemia- Reperfusion Injury
Current Drug Targets Glyco-Engineering of Human IgG-Fc to Modulate Biologic Activities
Current Pharmaceutical Biotechnology Thyroid Hormones Crosstalk with Growth Factors: Old Facts and New Hypotheses
Immunology, Endocrine & Metabolic Agents in Medicinal Chemistry (Discontinued)