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Induction of Brain-Derived Neurotrophic Factor in Plaque-Associated Glial Cells of Aged APP23 Transgenic Mice
Open accessAbstract
Brain-derived neurotrophic factor (BDNF) is a versatile neurotrophic factor that has been implicated in cell survival, cell differentiation, axonal growth, and activity-dependent synaptic plasticity. Changes in BDNF expression have also been reported during the course of several neurological disorders, including Alzheimer's disease (AD). The role of BDNF in AD, however, has remained elusive. To learn more about this neurotrophic factor, we investigated BDNF expression in brain of amyloid precursor protein overexpressing mice (APP23 transgenic mice).In situ hybridization revealed BDNF mRNA signals associated with amyloid plaques. Laser microdissection in combination with quantitative RT-PCR demonstrated a sixfold increase of BDNF mRNA in the immediate plaque vicinity, a threefold increase in a tissue ring surrounding the plaque, and control levels in interplaque areas comparable with those measured in age-matched nontransgenic mice. Double immunofluorescence localized BDNF to microglial cells and astrocytes surrounding the plaque. Cortical BDNF protein levels were quantified by ELISA demonstrating a >10-fold increase compared with age-matched controls. This upregulation of BDNF protein significantly correlated with the β-amyloid load in the transgenic animals. Taken together, our data demonstrate a plaque-associated upregulation of BDNF in APP23 transgenic mice and implicate this neurotrophin in the regulation of inflammatory and axonal growth processes in the plaque vicinity.
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“Previous work has shown BDNF expression is increased in amyloid-associated astrocytes (51)”
From Attenuating astrocyte activation accelerates plaque pathogenesis in APP/PS1 mice (2013) · cites this paper as [51]
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Metadata
- Authors
- Burbach, G. J., Hellweg, R., Haas, C. A., Del Turco, D., Deicke, U., Abramowski, D., Jucker, M., Staufenbiel, M., & Deller, T.
- Affiliations
- Goethe University Frankfurt (DE)
- Charité – Universitätsmedizin Berlin (DE)
- University of Freiburg (DE)
- Hertie Institute for Clinical Brain Research (DE)
- Corresponding author
- Deller, Thomas
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2004-03-10
- Volume
- 24
- Issue
- 10
- Pages
- 2421-2430
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6729483
- OpenAlex
- W2126869810
- Cited by
- 132
- References
- 77
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 3 · 2023: 8 · 2022: 2 · 2021: 6 · 2020: 12 · 2019: 5 · 2018: 4 · 2017: 3 · 2016: 9 · 2015: 2 · 2014: 6 · 2013: 6 · 2012: 6
- FWCI
- 3.92
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Alzheimer Forschung Initiative
- Deutsche Forschungsgemeinschaft (SFB 269)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- brain-derived neurotrophic factor, Alzheimer's disease, amyloid plaques, APP23 transgenic mice, microglia, astrocytes, amyloid-beta, neuroinflammation, axon growth, neurotrophic factor expression, aging
- MeSH terms
- Age Factors, Alzheimer Disease, Animals, Disease Models, Animal, Frontal Lobe, Mice, Transgenic, Neuroglia, Peptide Fragments, RNA, Messenger, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, In Situ Hybridization, Presynaptic Terminals, Brain-Derived Neurotrophic Factor, Mice, Plaque, Amyloid
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