Cited by 133Alzheimer's disease research and treatmentsNerve injury and regenerationNeuroinflammation and Neurodegeneration Mechanisms

Induction of Brain-Derived Neurotrophic Factor in Plaque-Associated Glial Cells of Aged APP23 Transgenic Mice

Open access
Burbach, Guido J., Hellweg, Rainer, Haas, Carola A., Del Turco, Domenico, Deicke, Uwe, Abramowski, Dorothee, Jucker, Mathias, Staufenbiel, Matthias +1 more·2004·The Journal of Neuroscience

Abstract

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.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1523/jneurosci.5599-03.2004

Cites

75 of 75 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

2 of the 77 references couldn’t be matched to a known paper.

Cited by

Sorted by citations

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
Published
2004-03-10
Volume
24
Issue
10
Pages
2421-2430
ISSN
  • 0270-6474 (ISSN-L)
  • 1529-2401
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
Locations
  • Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Alzheimer Forschung Initiative
  • Deutsche Forschungsgemeinschaft (SFB 269)
Topics
  • Health Sciences › Medicine › Physiology › 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

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review