Evidence map›Paper›PMID 26724934›Full record

ArticleActa neuropathologica2016

Neuroinflammation impairs adaptive structural plasticity of dendritic spines in a preclinical model of Alzheimer's disease.

Chengyu Zou, Yuan Shi, Jasmin Ohli, Ulrich Schüller, Mario M Dorostkar, Jochen Herms

Open access · hybridAbstract read
In one paragraph

Article in Acta neuropathologica, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 2 pooled it
5.1field-weighted citation impact, top 5% 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

34 citing papers in PubMed, 2 syntheses or guidelines pooled it, 64 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Article
  6. Targeting BACE1-mediated production of amyloid beta improves hippocampal synaptic function in an experimental model of ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023
    Article
  7. Review
  8. Antidiabetic Drugs in the Treatment of Alzheimer's Disease.International journal of molecular sciences · 2022
    Review
  9. Review
  10. Structural Plasticity of the Hippocampus in Neurodegenerative Diseases.International journal of molecular sciences · 2022
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. The p38Frontiers in cell and developmental biology · 2021
    Review
  17. Article
  18. Review
  19. Review
  20. Review
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

6 authors at 1 institution in 1 country.

Chengyu ZouDepartment for Translational Brain Research, German Center for Neurodegenerative Diseases (DZNE), Munich, Germany.
Yuan ShiDepartment for Translational Brain Research, German Center for Neurodegenerative Diseases (DZNE), Munich, Germany.
Jasmin OhliCenter for Neuropathology and Prion Research, Ludwig-Maximilians-University, Munich, Germany.
Ulrich SchüllerCenter for Neuropathology and Prion Research, Ludwig-Maximilians-University, Munich, Germany.
Mario M DorostkarCenter for Neuropathology and Prion Research, Ludwig-Maximilians-University, Munich, Germany.
Jochen HermsDepartment for Translational Brain Research, German Center for Neurodegenerative Diseases (DZNE), Munich, Germany. jochen.herms@med.uni-muenchen.de.
Ludwig-Maximilians-Universität München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To successfully treat Alzheimer's disease (AD), pathophysiological events in preclinical stages need to be identified. Preclinical AD refers to the stages that exhibit amyloid deposition in the brain but have normal cognitive function, which are replicated in young adult APPswe/PS1deltaE9 (deltaE9) mice. By long-term in vivo two-photon microscopy, we demonstrate impaired adaptive spine plasticity in these transgenic mice illustrated by their failure to increase dendritic spine density and form novel neural connections when housed in enriched environment (EE). Decrease of amyloid plaques by reducing BACE1 activity restores the gain of spine density upon EE in deltaE9 mice, but not the remodeling of neural networks. On the other hand, anti-inflammatory treatment with pioglitazone or interleukin 1 receptor antagonist in deltaE9 mice successfully rescues the impairments in increasing spine density and remodeling of neural networks during EE. Our data suggest that neuroinflammation disrupts experience-dependent structural plasticity of dendritic spines in preclinical stages of AD.

Indexed as

Alzheimer DiseaseAmyloid Precursor Protein SecretasesAnimalsAnti-Inflammatory AgentsAspartic Acid EndopeptidasesDendritic SpinesDisease Models, AnimalFemaleMice, Inbred C57BLMice, TransgenicNeuroimmunomodulationNeuronal PlasticityPioglitazonePyramidal CellsReceptors, Interleukin-1 Type ISomatosensory CortexAmyloid Precursor Protein SecretasesAnti-Inflammatory AgentsAspartic Acid EndopeptidasesBace1 protein, mousePioglitazoneReceptors, Interleukin-1 Type IThiazolidinedionesAPPswe/PS1deltaE9 miceDendritic spinesNeuroinflammationPreclinical ADStructural plasticity

Identifiers

PMID26724934
PMCPMC4713725
OpenAlexW2205716366

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.