Evidence map›Paper›PMID 28205565›Full record

ArticleScientific reports2017

Entorhinal Cortex dysfunction can be rescued by inhibition of microglial RAGE in an Alzheimer's disease mouse model.

Chiara Criscuolo, Veronica Fontebasso, Silvia Middei, Martina Stazi, Martine Ammassari-Teule, Shirley ShiDu Yan, Nicola Origlia

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

50 citing papers in PubMed, 78 citations in OpenAlex.

  1. Review
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  10. Receptors on Microglia.Advances in neurobiology · 2024
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  11. Synapse Regulation.Advances in neurobiology · 2024
    Review
  12. Synaptic Compensatory Plasticity in Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Review
  13. Age-Dependent Sex Differences in Perineuronal Nets in anInternational journal of molecular sciences · 2023
    Article
  14. Article
  15. The Inflammatory GeneBiomedicines · 2023
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  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

7 authors at 3 institutions in 2 countries.

Chiara CriscuoloNeuroscience Institute, Italian National Research Council, Pisa, 56100 Pisa, Italy.
Veronica FontebassoInstitute of Cell Biology and Neurobiology, Italian National Research Council, Roma, 00143 Roma, Italy.
Silvia MiddeiInstitute of Cell Biology and Neurobiology, Italian National Research Council, Roma, 00143 Roma, Italy.
Martina StaziNeuroscience Institute, Italian National Research Council, Pisa, 56100 Pisa, Italy.
Martine Ammassari-TeuleInstitute of Cell Biology and Neurobiology, Italian National Research Council, Roma, 00143 Roma, Italy.
Shirley ShiDu YanDepartment of Pharmacology and Toxicology, University of Kansas, Lawrence, KS 66045, USA.
Nicola OrigliaNeuroscience Institute, Italian National Research Council, Pisa, 56100 Pisa, Italy.
National Research Council · ITNeuroscience Institute · ITUniversity of Kansas · US

Funding

Mitochondrial degrading enzyme, synaptic mitochondrial function in AD mouse modelR01AG044793 · NIA · UNIVERSITY OF KANSAS LAWRENCE · PI YAN, SHIRLEY SHIDU · 2014 to 2018
$1.9M
RAGE and mitochondrial degeneration in diabetesR01NS089116 · NINDS · UNIVERSITY OF KANSAS LAWRENCE · PI YAN, SHIRLEY SHIDU · 2015 to 2018
$1.5M
Austrian Science Fund FWF P 28146NIA NIH HHS R01 AG044793NINDS NIH HHS R01 NS089116
6 · The paper itself

Abstract

The Entorhinal cortex (EC) has been implicated in the early stages of Alzheimer's disease (AD). In particular, spreading of neuronal dysfunction within the EC-Hippocampal network has been suggested. We have investigated the time course of EC dysfunction in the AD mouse model carrying human mutation of amyloid precursor protein (mhAPP) expressing human Aβ. We found that in mhAPP mice plasticity impairment is first observed in EC superficial layer and further affected with time. A selective impairment of LTP was observed in layer II horizontal connections of EC slices from 2 month old mhAPP mice, whereas at later stage of neurodegeneration (6 month) basal synaptic transmission and LTD were also affected. Accordingly, early synaptic deficit in the mhAPP mice were associated with a selective impairment in EC-dependent associative memory tasks. The introduction of the dominant-negative form of RAGE lacking RAGE signalling targeted to microglia (DNMSR) in mhAPP mice prevented synaptic and behavioural deficit, reducing the activation of stress related kinases (p38MAPK and JNK). Our results support the involvement of the EC in the development and progression of the synaptic and behavioural deficit during amyloid-dependent neurodegeneration and demonstrate that microglial RAGE activation in presence of Aβ-enriched environment contributes to the EC vulnerability.

Indexed as

Alzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsBehavior, AnimalDendritic SpinesDisease Models, AnimalEntorhinal CortexHumansJNK Mitogen-Activated Protein KinasesMice, Inbred C57BLMice, TransgenicMicrogliaMutationNerve DegenerationNeuronal Plasticityp38 Mitogen-Activated Protein KinasesAmyloid beta-Protein PrecursorJNK Mitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesReceptor for Advanced Glycation End Products

Identifiers

PMID28205565
PMCPMC5304222
OpenAlexW2588124790

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.