Aggregation-Dependent Interaction of the Alzheimers β-Amyloid and Microglia
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Frank Muehlhauser
Abstract
Chronic glial activation possibly plays a role in chronic neurodegeneration in Alzheimer's disease (AD). It has been shown that amyloid peptide is capable of activating microglial cells in vitro. The aim of this study was to further characterize the structural preconditions for amyloid peptide in order to activate glial cells and to investigate whether this peptide is also able to induce glial activation in the living brain.
We observed that amyloid peptide induced strong cellular activation in primary microglial cell culture as detected by the release of stable metabolites of nitric oxide (NO), when the peptide was fibrillar. For this activation, co-stimulation with interferon-γ was a precondition. Using microdialysis of the living brain in a rat we observed pronounced NO generation when fibrillar amyloid peptide was stereotaxically injected. Non-fibrillar amyloid peptide did not induce such a glial reaction. No administration of interferon-γ or any other co-stimulatory factor was necessary in vivo.
Thus, we show that fibrillar, but not non-fibrillar amyloid peptide induced glial activation also in vivo. In the case of the living brain, the presence of deposits of fibrillar amyloid peptide could maintain a chronic microglial activation, ultimately leading to the progressive neurodegeneration associated with Alzheimer's disease.
Copyright © 2001 by Walter de Gruyter GmbH & Co. KG
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- Polymorphism of Apoprotein E (APOE), Methylenetetrahydrofolate Reductase (MTHFR) and Paraoxonase (PON1) Genes in Patients with Cerebrovascular Disease
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Articles in the same Issue
- IFCC/ Beckman Coulter Inc. Conference Frontiers in Molecular Basis of Diseases: Cell Biology of Neuronal Dysfunction, Paris, October 12-13, 2000
- Distribution of Cellular Prion Protein in Normal Human Cerebral Cortex – Does It Have Relevance to Creutzfeldt-Jakob Disease?
- Caspase-3 Apoptotic Signaling Following Injury to the Central Nervous System
- Parkinsons Disease and other α-Synucleinopathies
- Aggregation-Dependent Interaction of the Alzheimers β-Amyloid and Microglia
- β-Amyloid-Induced Cytotoxicity, Peroxide Generation and Blockade of Glutamate Uptake in Cultured Astrocytes
- Protein S-100B: A Serum Marker for Ischemic and Infectious Injury of Cerebral Tissue
- Reporting Cerebrospinal Fluid Data: Knowledge Base and Interpretation Software
- The Intrathecal Humoral Immune Response: Laboratory Analysis and Clinical Relevance
- Source of Endothelin-1 in Subarachnoid Hemorraghe
- Polymorphism of Apoprotein E (APOE), Methylenetetrahydrofolate Reductase (MTHFR) and Paraoxonase (PON1) Genes in Patients with Cerebrovascular Disease
- Neurotrophic Factor Therapy – Prospects and Problems
- Cell Therapy and Transplantation in Parkinsons Disease
- Matrix Metalloproteinases: Potential Therapeutic Target in Spinal Cord Injury
