Evidence map›Paper›PMID 27544234›Full record

ArticleMolecular neurobiology2016

Early Changes in Hippocampal Neurogenesis in Transgenic Mouse Models for Alzheimer's Disease.

M S Unger, J Marschallinger, J Kaindl, C Höfling, S Rossner, Michael T Heneka, A Van der Linden, Ludwig Aigner

Open access · hybridAbstract read
In one paragraph

Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

54 citing papers in PubMed, 88 citations in OpenAlex.

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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 3 countries.

M S UngerInstitute of Molecular Regenerative Medicine, Paracelsus Medical University, Strubergasse 21, 5020, Salzburg, Austria.
J MarschallingerInstitute of Molecular Regenerative Medicine, Paracelsus Medical University, Strubergasse 21, 5020, Salzburg, Austria.
J KaindlInstitute of Molecular Regenerative Medicine, Paracelsus Medical University, Strubergasse 21, 5020, Salzburg, Austria.
C HöflingPaul Flechsig Institute for Brain Research, University of Leipzig, Leipzig, Germany.
S RossnerPaul Flechsig Institute for Brain Research, University of Leipzig, Leipzig, Germany.
Michael T HenekaClinical Neuroscience, Department of Neurology, University of Bonn, Bonn, Germany.
A Van der LindenDepartment of Biomedical Sciences, University of Antwerp, Antwerp, Belgium.
Ludwig AignerInstitute of Molecular Regenerative Medicine, Paracelsus Medical University, Strubergasse 21, 5020, Salzburg, Austria. ludwig.aigner@pmu.ac.at.
Paracelsus Medical University · ATLeipzig University · DEUniversity of Antwerp · BEUniversity of Bonn · DE

Funding

Austrian Science Fund FWF F 4413
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most prevalent neurodegenerative disease in the Western world and is characterized by a progressive loss of cognitive functions leading to dementia. One major histopathological hallmark of AD is the formation of amyloid-beta plaques, which is reproduced in numerous transgenic animal models overexpressing pathogenic forms of amyloid precursor protein (APP). In human AD and in transgenic amyloid plaque mouse models, several studies report altered rates of adult neurogenesis, i.e. the formation of new neurons from neural stem and progenitor cells, and impaired neurogenesis has also been attributed to contribute to the cognitive decline in AD. So far, changes in neurogenesis have largely been considered to be a consequence of the plaque pathology. Therefore, possible alterations in neurogenesis before plaque formation or in prodromal AD have been largely ignored. Here, we analysed adult hippocampal neurogenesis in amyloidogenic mouse models of AD at different points before and during plaque progression. We found prominent alterations of hippocampal neurogenesis before plaque formation. Survival of newly generated cells and the production of new neurons were already compromised at this stage. Moreover and surprisingly, proliferation of doublecortin (DCX) expressing neuroblasts was significantly and specifically elevated during the pre-plaque stage in the APP-PS1 model, while the Nestin-expressing stem cell population was unaffected. In summary, changes in neurogenesis are evident already before plaque deposition and might contribute to well-known early hippocampal dysfunctions in prodromal AD such as hippocampal overactivity.

Indexed as

NeurogenesisAlzheimer DiseaseAnimalsCell CountCell LineageCell ProliferationCell SurvivalDentate GyrusDisease Models, AnimalDoublecortin Domain ProteinsDoublecortin ProteinFemaleHippocampusMice, TransgenicMicrotubule-Associated ProteinsNeuronsDCX protein, humanDcx protein, mouseDoublecortin Domain ProteinsDoublecortin ProteinMicrotubule-Associated ProteinsNeuropeptidesAlzheimer’s diseaseNeural stem- and progenitorsNeurogenesis

Identifiers

PMID27544234
PMCPMC5012146
OpenAlexW2508146274

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.