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Inhibition of Microglial Activation Protects Hippocampal Neurogenesis and Improves Cognitive Deficits in a Transgenic Mouse Model for Alzheimer’s Disease
Open accessAbstract
Background: Activated microglia with macrophage-like functions invade and surround β-amyloid (Aβ) plaques in Alzheimer’s disease (AD), possibly contributing to the turnover of Aβ, but they can also secrete proinflammatory factors that may be involved in the pathogenesis of AD. Microglia are known to modulate adult hippocampal neurogenesis. Objectives/Methods: To determine the role of microglia on neurogenesis in brains with Aβ pathology, we inhibited microglial activation with the tetracycline derivative minocycline in doubly transgenic mice expressing mutant human amyloid precursor protein (APP) and mutant human presenilin-1 (PS1). Results: Minocycline increased the survival of new dentate granule cells in APP/PS1 mice indicated by more BrdU+/NeuN+ cells as compared to vehicle-treated transgenic littermates, accompanied by improved behavioral performance in a hippocampus-dependent learning task. Both brain levels of Aβ and Aβ-related morphological deficits in the new neurons labeled with GFP-expressing retrovirus were unaffected in minocycline-treated mice. Conclusions: These results suggest a role for microglia in Aβ-related functional deficits and in suppressing the survival of new neurons, and show that modulation of microglial function with minocycline can protect hippocampal neurogenesis in the presence of Aβ pathology.
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“treatment with antiinflammatory medication tends to mitigate cognitive impairment in animal models of amyloid-β injection [149, 150].”
From Brain-Derived Neurotrophic Factor in Brain Disorders: Focus on Neuroinflammation (2019) · cites this paper as [150]
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Metadata
- Authors
- Biscaro, B., Lindvall, O., Tesco, G., Ekdahl, C. T., & Nitsch, R. M.
- Affiliations
- University of Zurich (CH)
- Lund University (SE)
- Tufts University (US)
- Venue
- Neurodegenerative Diseases
- Publisher
- S. Karger AG
- Published
- 2012
- Volume
- 9
- Issue
- 4
- Pages
- 187-198
- ISSN
- 1660-2854 (ISSN-L)
- 1660-2862
- PMC
- PMC7068786
- OpenAlex
- W2003614844
- Cited by
- 164
- References
- 48
- Citations by year
- 2026: 4 · 2025: 8 · 2024: 7 · 2023: 8 · 2022: 14 · 2021: 7 · 2020: 13 · 2019: 14 · 2018: 11 · 2017: 12 · 2016: 7 · 2015: 20 · 2014: 17 · 2013: 16 · 2012: 6
- FWCI
- 9.49
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Neurodegenerative Diseases (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Zurich Open Repository and Archive (University of Zurich) (acceptedVersion, other-oa)
- Lund University Publications (Lund University) (submittedVersion)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion, other-oa)
- Zurich Open Repository and Archive (University of Zurich)
- Funders
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
- Vetenskapsrådet
- National Institute on Aging (R01AG033016, R01AG025952)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- microglial activation, hippocampal neurogenesis, Alzheimer's disease, minocycline, amyloid-beta, APP/PS1 mice, dentate gyrus granule cells, cognitive impairment, neuroinflammation
- MeSH terms
- Alzheimer Disease, Animals, Anti-Inflammatory Agents, Cognition Disorders, Disease Models, Animal, Female, Hippocampus, Humans, Male, Mice, Inbred C57BL, Mice, Transgenic, Minocycline, Mutation, Amyloid beta-Protein Precursor, Microglia, Mice, Presenilin-1, Neurogenesis
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