Evidence map›Paper›PMID 29855361›Full record

ArticleActa neuropathologica communications2018

Environmental enrichment reverses Aβ pathology during pregnancy in a mouse model of Alzheimer's disease.

Stephanie Ziegler-Waldkirch, Karin Marksteiner, Johannes Stoll, Paolo d'Errico, Marina Friesen, Denise Eiler, Lea Neudel, Verena Sturn, Isabel Opper, Moumita Datta and 2 more

Open access · goldAbstract read
In one paragraph

Article in Acta neuropathologica communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

13 citing papers in PubMed, 27 citations in OpenAlex.

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  11. Multiparity, Brain Atrophy, and Cognitive Decline.Frontiers in aging neuroscience · 2020
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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

12 authors at 1 institution in 1 country.

Stephanie Ziegler-WaldkirchDepartment of Neurology, Medical Center - University of Freiburg, Freiburg, Germany.
Karin MarksteinerDepartment of Neurology, Medical Center - University of Freiburg, Freiburg, Germany.
Johannes StollDepartment of Neurology, Medical Center - University of Freiburg, Freiburg, Germany.
Paolo d'ErricoDepartment of Neurology, Medical Center - University of Freiburg, Freiburg, Germany.
Marina FriesenDepartment of Neurology, Medical Center - University of Freiburg, Freiburg, Germany.
Denise EilerDepartment of Neurology, Medical Center - University of Freiburg, Freiburg, Germany.
Lea NeudelDepartment of Neurology, Medical Center - University of Freiburg, Freiburg, Germany.
Verena SturnDepartment of Neurology, Medical Center - University of Freiburg, Freiburg, Germany.
Isabel OpperDepartment of Neurology, Medical Center - University of Freiburg, Freiburg, Germany.
Moumita DattaFaculty of Medicine, University of Freiburg, Freiburg, Germany.
Marco PrinzFaculty of Medicine, University of Freiburg, Freiburg, Germany.
Melanie Meyer-LuehmannDepartment of Neurology, Medical Center - University of Freiburg, Freiburg, Germany. melanie.meyer-luehmann@uniklinik-freiburg.de.ORCID 0000-0003-3661-2220
University of Freiburg · DE

Funding

Deutsche Forschungsgemeinschaft ME 3542/2-1Deutsche Forschungsgemeinschaft 'NeuroMac' Graduate School of the SFB/TRR 167
6 · The paper itself

Abstract

Several studies suggest that women have a higher risk to develop Alzheimer's disease (AD) than men. In particular, the number of pregnancies was shown to be a risk factor for AD and women with several pregnancies on average had an earlier onset of the disease, thus making childbearing a risk factor. However, the impact of being pregnant on Aβ plaque pathology and adult neurogenesis still remains elusive. Postmortem analysis revealed that pregnant 5xFAD transgenic mice had significantly more Aβ plaques in the hippocampus from G10 onwards and that the number of Ki67 and DCX positive cells dramatically decreased during the postpartum period. Furthermore, 5 months old 5xFAD transgenic mice that also nursed their offsprings for 4 weeks had a similar Aβ plaque load than merely pregnant mice, indicating that pregnancy alone is sufficient to elevate Aβ plaque levels. Interestingly, housing in an enriched environment reduced the Aβ plaque load and vivified neurogenesis. Our results suggest that pregnancy alters Aβ plaque deposition in 5xFAD transgenic mice and diminishes the generation of newborn neurons. We conclude that pregnancy alone is sufficient to induce this phenotype that can be reversed upon environmental enrichment.

Indexed as

EnvironmentAlzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsDisease Models, AnimalDoublecortin Domain ProteinsDoublecortin ProteinFemaleHippocampusHumansKi-67 AntigenLactationMiceMice, Inbred C57BLMice, TransgenicAmyloid beta-Peptidesamyloid beta-protein (1-40)amyloid beta-protein (1-42)Amyloid beta-Protein PrecursorDCX protein, humanDcx protein, mouseDoublecortin Domain ProteinsDoublecortin ProteinKi-67 AntigenMicrotubule-Associated ProteinsNeuropeptidesPeptide FragmentsPresenilin-1PSEN1 protein, humanThomsen-Friedenreich antigen, crypticTrisaccharidesAdult neurogenesisAlzheimer’s diseaseAmyloid-β plaquesEnvironmental enrichmentEstrogensPregnancyProgesterone

Identifiers

PMID29855361
PMCPMC5984325
OpenAlexW2806518113

What OpenQuestion holds

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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.