Evidence map›Paper›PMID 33588898›Full record

ReviewMolecular neurodegeneration2021

Remodeling Alzheimer-amyloidosis models by seeding.

Brittany S Ulm, David R Borchelt, Brenda D Moore

Open access · goldAbstract readReview
In one paragraph

Review in Molecular neurodegeneration, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

15 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Updates on mouse models of Alzheimer's disease.Molecular neurodegeneration · 2024
    Review
  12. Review
  13. Article
  14. Article
  15. 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

3 authors at 1 institution in 1 country.

Brittany S UlmDepartment of Neuroscience, Center for Translational Research in Neurodegenerative Disease, McKnight Brain Institute, College of Medicine, University of Florida, Gainesville, FL, USA.
David R BorcheltDepartment of Neuroscience, Center for Translational Research in Neurodegenerative Disease, McKnight Brain Institute, College of Medicine, University of Florida, Gainesville, FL, USA.
Brenda D MooreDepartment of Neuroscience, Center for Translational Research in Neurodegenerative Disease, McKnight Brain Institute, College of Medicine, University of Florida, Gainesville, FL, USA. brendar@ufl.edu.ORCID 0000-0002-9685-6561
University 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
Elucidating factors that modulate tauopathy and cellular degeneration to guide therapeutic developmentRF1AG064914 · NIA · UNIVERSITY OF FLORIDA · PI GOLDE, TODD E, LEWIS, JADA M · 2019 to 2019
$2.5M
Clinical and Translational Predoctoral training in Alzheimers Disease and Related DementiasT32AG061892 · NIA · UNIVERSITY OF FLORIDA · PI PARAMITA CHAKRABARTY, JADA M LEWIS · 2018 to 2026
$1.8M
Proteostasis and secondary proteinopathy in AD and FTDR01AG049456 · NIA · UNIVERSITY OF FLORIDA · PI BORCHELT, DAVID R, LEWIS, JADA M · 2015 to 2019
$1.5M
Is there a form of benign brain amyloidosis in aging?R21AG055113 · NIA · UNIVERSITY OF FLORIDA · PI BORCHELT, DAVID R, LEWIS, JADA M · 2017 to 2018
$419k
NIA NIH HHS P50 AG047266NIA NIH HHS R01 AG049456NIA NIH HHS R21 AG055113NIA NIH HHS RF1 AG064914NIA NIH HHS T32 AG061892
6 · The paper itself

Abstract

Alzheimer's disease (AD) is among the most prevalent neurodegenerative diseases, with brain pathology defined by extracellular amyloid beta deposits and intracellular tau aggregates. To aid in research efforts to improve understanding of this disease, transgenic murine models have been developed that replicate aspects of AD pathology. Familial AD is associated with mutations in the amyloid precursor protein and in the presenilins (associated with amyloidosis); transgenic amyloid models feature one or more of these mutant genes. Recent advances in seeding methods provide a means to alter the morphology of resultant amyloid deposits and the age that pathology develops. In this review, we discuss the variety of factors that influence the seeding of amyloid beta pathology, including the source of seed, the time interval after seeding, the nature of the transgenic host, and the preparation of the seeding inoculum.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAmyloidosisAnimalsBrainDisease Models, AnimalHumansAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAlzheimer’s diseaseAmyloid-βMouse modelsPrion diseaseSeeding

Identifiers

PMID33588898
PMCPMC7885558
OpenAlexW3131317233

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.