Evidence map›Paper›PMID 28059792›Full record

ArticleJournal of Alzheimer's disease : JAD2017

Quantitative Comparison of Dense-Core Amyloid Plaque Accumulation in Amyloid-β Protein Precursor Transgenic Mice.

Peng Liu, John H Reichl, Eshaan R Rao, Brittany M McNellis, Eric S Huang, Laura S Hemmy, Colleen L Forster, Michael A Kuskowski, David R Borchelt, Robert Vassar and 2 more

Open access · greenAbstract readComparative Study
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 20% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
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  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. White Button Mushroom (Brain sciences · 2022
    Article
  11. Article
  12. Article
  13. Review
  14. Remodeling Alzheimer-amyloidosis models by seeding.Molecular neurodegeneration · 2021
    Review
  15. Article
  16. The biogenesis and biology of amyloid β oligomers in the brain.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2020
    Review
  17. Article
  18. Article
  19. Article
  20. Article
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 4 institutions in 1 country.

Peng LiuDepartment of Neurology, University of Minnesota, Minneapolis, MN, USA.
John H ReichlDepartment of Neurology, University of Minnesota, Minneapolis, MN, USA.
Eshaan R RaoN. Bud Grossman Center for Memory Research and Care, University of Minnesota, Minneapolis, MN, USA.
Brittany M McNellisN. Bud Grossman Center for Memory Research and Care, University of Minnesota, Minneapolis, MN, USA.
Eric S HuangDepartment of Neurology, University of Minnesota, Minneapolis, MN, USA.
Laura S HemmyDepartment of Psychiatry, University of Minnesota, Minneapolis, MN, USA.
Colleen L ForsterN. Bud Grossman Center for Memory Research and Care, University of Minnesota, Minneapolis, MN, USA.
Michael A KuskowskiDepartment of Psychiatry, University of Minnesota, Minneapolis, MN, USA.
David R BorcheltDepartment of Neuroscience, University of Florida, Gainesville, FL, USA.
Robert VassarDepartment of Cellular and Molecular Biology, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
Karen H AsheDepartment of Neurology, University of Minnesota, Minneapolis, MN, USA.
Kathleen R ZahsDepartment of Neurology, University of Minnesota, Minneapolis, MN, USA.
University of Minnesota · USGeriatric Research Education and Clinical Center · USNorthwestern University · USUniversity of Florida · US

Funding

University of Florida - Mt. Sinai Medical Center AD Research CenterP50AG047266 · NIA · UNIVERSITY OF FLORIDA · PI FEBO, MARCELO · 2015 to 2019
$7.3M
TOWARD A MODEL OF ALZHEIMERS DISEASER01NS033249 · NINDS · UNIVERSITY OF MINNESOTA TWIN CITIES · PI ASHE, KAREN H · 1994 to 2013
$6.5M
INDEPENDENT AND DEPENDENT LIFE IN THE ELDERLYR01AG009862 · NIA · UNIVERSITY OF KENTUCKY · PI SNOWDON, DAVID A. · 1990 to 2006
$6.1M
BACE1 as a Therapeutic Target for Alzheimer's DiseaseR01AG022560 · NIA · NORTHWESTERN UNIVERSITY AT CHICAGO · PI VASSAR, ROBERT J · 2003 to 2017
$4.6M
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
Training in Emerging Multidisciplinary Approaches to Mental Health and DiseaseT32MH020065 · NIMH · UNIVERSITY OF CHICAGO · PI NICOLAE, DAN LIVIU, RZHETSKY, ANDREY · 2002 to 2017
$2.3M
BACE1 as a Therapeutic Target for Alzheimer's DiseaseRF1AG022560 · NIA · NORTHWESTERN UNIVERSITY AT CHICAGO · PI VASSAR, ROBERT J · 2019 to 2019
$2.0M
NIA NIH HHS P50 AG047266NIA NIH HHS R01 AG009862NIA NIH HHS R01 AG022560NIA NIH HHS R01 AG030142NIA NIH HHS RF1 AG022560NIMH NIH HHS T32 MH020065NINDS NIH HHS R01 NS033249
6 · The paper itself

Abstract

There exist several dozen lines of transgenic mice that express human amyloid-β protein precursor (AβPP) with Alzheimer's disease (AD)-linked mutations. AβPP transgenic mouse lines differ in the types and amounts of Aβ that they generate and in their spatiotemporal patterns of expression of Aβ assemblies, providing a toolkit to study Aβ amyloidosis and the influence of Aβ aggregation on brain function. More complete quantitative descriptions of the types of Aβ assemblies present in transgenic mice and in humans during disease progression should add to our understanding of how Aβ toxicity in mice relates to the pathogenesis of AD. Here, we provide a direct quantitative comparison of amyloid plaque burdens and plaque sizes in four lines of AβPP transgenic mice. We measured the fraction of cortex and hippocampus occupied by dense-core plaques, visualized by staining with Thioflavin S, in mice from young adulthood through advanced age. We found that the plaque burdens among the transgenic lines varied by an order of magnitude: at 15 months of age, the oldest age studied, the median cortical plaque burden in 5XFAD mice was already ∼4.5 times that of 21-month-old Tg2576 mice and ∼15 times that of 21-24-month-old rTg9191 mice. Plaque-size distributions changed across the lifespan in a line- and region-dependent manner. We also compared the dense-core plaque burdens in the mice to those measured in a set of pathologically-confirmed AD cases from the Nun Study. Cortical plaque burdens in Tg2576, APPSwePS1ΔE9, and 5XFAD mice eventually far exceeded those measured in the human cohort.

Indexed as

Aged, 80 and overAgingAlzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsBenzothiazolesCerebral CortexDisease Models, AnimalFemaleHippocampusHumansMaleMice, TransgenicPlaque, AmyloidSpecies SpecificityThiazolesAmyloid beta-Protein PrecursorAPP protein, humanBenzothiazolesThiazolesthioflavin TAlzheimer’s diseaseamyloid plaqueamyloid-β protein precursorplaque burdenplaque sizeThioflavin Stransgenic mouse

Identifiers

PMID28059792
PMCPMC5272806
OpenAlexW2569997965

What OpenQuestion holds

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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.