Evidence map›Paper›PMID 30315100›Full record

ArticleThe Journal of biological chemistry2018

ER stress is not elevated in the 5XFAD mouse model of Alzheimer's disease.

Katherine R Sadleir, Jelena Popovic, Robert Vassar

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

35 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
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  6. Review
  7. Article
  8. Peripheral HMGB1 is linked to OAlzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  9. Genetic diversity promotes resilience in a mouse model of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
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  14. Review
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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

3 authors at 1 institution in 1 country.

Katherine R SadleirFrom the Department of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611.ORCID 0000-0001-8310-841X
Jelena PopovicFrom the Department of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611.
Robert VassarFrom the Department of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611 r-vassar@northwestern.edu.
Northwestern University · US

Funding

Molecular Neuropathology and Mechanisms of BACE1 Elevation in Alzheimer's DiseaseR01AG030142 · NIA · NORTHWESTERN UNIVERSITY AT CHICAGO · PI VASSAR, ROBERT J · 2007 to 2019
$3.1M
NIA NIH HHS R01 AG030142
6 · The paper itself

Abstract

Alzheimer's disease mouse models that overexpress amyloid precursor protein (APP) and presenilin 1 (PS1) form β-amyloid (Aβ) plaques, a hallmark Alzheimer's disease lesion. It has been assumed that the neuroinflammation, synaptic dysfunction, neurodegeneration, and cognitive impairment observed in these mice are caused by cerebral Aβ accumulation. However, it is also possible that accumulation of the overexpressed transmembrane proteins APP and PS1 in the endoplasmic reticulum (ER) triggers chronic ER stress and activation of the unfolded protein response (UPR). The 5XFAD mouse, a widely used amyloid pathology model, overexpresses APP and PS1, displays aggressive amyloid pathology, and has been reported to exhibit ER stress. To systematically evaluate whether 5XFAD mice have increased ER stress, here we used biochemical approaches to assess a comprehensive panel of UPR markers. We report that APP and PS1 levels are 1.8- and 1.5-fold, respectively, of those in 5XFAD compared with nontransgenic brains, indicating that transgenes are not massively overexpressed in 5XFAD mice. Using immunoblotting, we quantified UPR protein levels in nontransgenic, 5XFAD, and 5XFAD;BACE1

Indexed as

Disease Models, AnimalEndoplasmic Reticulum StressAlzheimer DiseaseAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesAnimalsAspartic Acid EndopeptidasesFemaleHumansMaleMiceMice, TransgenicMutationPresenilin-1Unfolded Protein ResponseAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesAspartic Acid EndopeptidasesBace1 protein, mousePresenilin-15XFADAlzheimer's diseaseamyloidamyloid precursor protein (APP)amyloid β (Aβ)endoplasmic reticulum stress (ER stress)mouse modelneurodegenerationprotein aggregationtransgenic mice

Identifiers

PMID30315100
PMCPMC6290164
OpenAlexW2896566631

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.