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Updated: Aug 6, 2026
Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus
Published on: June 17, 2015
Glial-derived Neuroinflammation induced with Amyloid-beta-peptide Plus Fibrinogen Injection in Rat Hippocampus
1Department of Anesthesiology, Pharmacology and Therapeutics, Faculty of Medicine, The University of British Columbia, 2176 Health Sciences Mall, Vancouver, BC, Canada V6T 1Z3.
Introduction:
The present study has examined microglial and astrocyte activation in association with neuronal degeneration in an animal model using an injection of amyloid-beta peptide Aβ1-42 (Aβ42) plus fibrinogen into rat hippocampus.
Methods:
The combination of stimuli is suggested as a novel and potent perturbation to induce gliosis and the production of glial-derived neurotoxic factors in an animal model exhibiting a leaky BBB (blood-brain barrier). Specifically, Aβ42 + fibrinogen stimulation elevated levels of COX-2 (cyclooxygenase-2) and iNOS (inducible nitric oxide synthase) with a considerable extent of neuronal loss associated with microglia and astrocyte activation.
Results:
Treatment of injected rats with the broad spectrum anti-inflammatory agent, minocycline or the iNOS inhibitor, 1400 W inhibited gliosis, reduced levels of COX-2 and iNOS, and demonstrated efficacy for neuroprotection.
Conclusion:
The findings suggest the utility of combining amyloid beta peptide plus fibrinogen as a potent and understudied neuroinflammatory stimulus for the induction of glial-derived neurotoxic factors in BBB-compromised AD brain.
Insights
Amyloid-beta and fibrinogen injection induced neuroinflammation and neuronal loss in rats. Anti-inflammatory treatments protected against this damage, suggesting a therapeutic target for Alzheimer's disease.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Microglial and astrocyte activation are key features of neuroinflammation.
- Amyloid-beta (Aβ) and fibrinogen can trigger neuroinflammatory responses.
Purpose of the Study:
- To investigate microglial and astrocyte activation in response to Aβ42 plus fibrinogen in a rat model.
- To evaluate the neuroprotective effects of anti-inflammatory agents.
Main Methods:
- Intrahippocampal injection of Aβ42 plus fibrinogen in rats.
- Administration of minocycline or the iNOS inhibitor 1400 W.
- Assessment of gliosis, COX-2, iNOS, and neuronal loss.
Main Results:
- Aβ42 + fibrinogen induced significant gliosis, elevated COX-2 and iNOS levels, and neuronal degeneration.
- Minocycline and 1400 W treatment inhibited gliosis and reduced neuroinflammation.
- Both treatments demonstrated neuroprotective effects.
Conclusions:
- Combining Aβ42 and fibrinogen is a potent stimulus for neuroinflammation in a compromised blood-brain barrier model.
- Targeting neuroinflammation with agents like minocycline or iNOS inhibitors shows therapeutic potential for Alzheimer's disease.
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