Evidence map›Paper›PMID 26881108›Full record

ArticleNeural plasticity2016

Amyloid-Beta Induced Changes in Vesicular Transport of BDNF in Hippocampal Neurons.

Bianca Seifert, Robert Eckenstaler, Raik Rönicke, Julia Leschik, Beat Lutz, Klaus Reymann, Volkmar Lessmann, Tanja Brigadski

Open access · goldAbstract read
In one paragraph

Article in Neural plasticity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 16% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 30 citations in OpenAlex.

  1. BDNF-amyloid-Frontiers in molecular neuroscience · 2026
    Review
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  3. Article
  4. Article
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  6. Article
  7. Article
  8. The physiology of regulated BDNF release.Cell and tissue research · 2020
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 1 country.

Bianca SeifertInstitute of Physiology, Medical Faculty, Otto-von-Guericke-University, 39120 Magdeburg, Germany.
Robert EckenstalerInstitute of Physiology, Medical Faculty, Otto-von-Guericke-University, 39120 Magdeburg, Germany.
Raik RönickeInstitute of Clinical Chemistry and Pathobiochemistry, Medical Faculty, Otto-von-Guericke-University, 39120 Magdeburg, Germany; German Center for Neurodegenerative Diseases (DZNE), 39120 Magdeburg, Germany.
Julia LeschikInstitute of Physiological Chemistry, University Medical Center of the Johannes Gutenberg University, 55128 Mainz, Germany.
Beat LutzInstitute of Physiological Chemistry, University Medical Center of the Johannes Gutenberg University, 55128 Mainz, Germany.
Klaus ReymannGerman Center for Neurodegenerative Diseases (DZNE), 39120 Magdeburg, Germany.
Volkmar LessmannInstitute of Physiology, Medical Faculty, Otto-von-Guericke-University, 39120 Magdeburg, Germany; Center of Behavioral Brain Sciences (CBBS), 39106 Magdeburg, Germany.
Tanja BrigadskiInstitute of Physiology, Medical Faculty, Otto-von-Guericke-University, 39120 Magdeburg, Germany; Center of Behavioral Brain Sciences (CBBS), 39106 Magdeburg, Germany.
Otto-von-Guericke University Magdeburg · DECenter for Behavioral Brain Sciences · DEUniversity Medical Center of the Johannes Gutenberg University Mainz · DEGerman Center for Neurodegenerative Diseases · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The neurotrophin brain derived neurotrophic factor (BDNF) is an important growth factor in the CNS. Deficits in transport of this secretory protein could underlie neurodegenerative diseases. Investigation of disease-related changes in BDNF transport might provide insights into the cellular mechanism underlying, for example, Alzheimer's disease (AD). To analyze the role of BDNF transport in AD, live cell imaging of fluorescently labeled BDNF was performed in hippocampal neurons of different AD model systems. BDNF and APP colocalized with low incidence in vesicular structures. Anterograde as well as retrograde transport of BDNF vesicles was reduced and these effects were mediated by factors released from hippocampal neurons into the extracellular medium. Transport of BDNF was altered at a very early time point after onset of human APP expression or after acute amyloid-beta(1-42) treatment, while the activity-dependent release of BDNF remained unaffected. Taken together, extracellular cleavage products of APP induced rapid changes in anterograde and retrograde transport of BDNF-containing vesicles while release of BDNF was unaffected by transgenic expression of mutated APP. These early transport deficits might lead to permanently impaired brain functions in the adult brain.

Indexed as

Amyloid beta-PeptidesAnimalsAnimals, NewbornBrain-Derived Neurotrophic FactorCells, CulturedHippocampusHumansMice, Inbred C57BLMice, TransgenicNeuronsPeptide FragmentsProtein TransportTransport VesiclesAmyloid beta-Peptidesamyloid beta-protein (1-42)Brain-Derived Neurotrophic FactorPeptide Fragments

Identifiers

PMID26881108
PMCPMC4736975
OpenAlexW2227163679

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.