Evidence map›Paper›PMID 31528297›Full record

ArticlePathobiology of aging & age related diseases2019

Cross species application of quantitative neuropathology assays developed for clinical Alzheimer's disease samples.

Silvan R Urfer, Caitlin S Latimer, Warren Ladiges, C Dirk Keene, Sarah Benbow, Benjamin Harrison, Daniel E L Promislow, Matt Kaeberlein, Brian C Kraemer, Adrienne Wang and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Pathobiology of aging & age related diseases, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

12 authors.

Silvan R UrferDepartment of Pathology, University of Washington, Seattle, WA, USA.ORCID 0000-0002-3722-0731
Caitlin S LatimerDepartment of Pathology, University of Washington, Seattle, WA, USA.
Warren LadigesDepartment of Comparative Medicine, University of Washington, Seattle, WA, USA.
C Dirk KeeneDepartment of Pathology, University of Washington, Seattle, WA, USA.
Sarah BenbowDepartment of Medicine, University of Washington, Seattle, WA, USA.
Benjamin HarrisonDepartment of Pathology, University of Washington, Seattle, WA, USA.
Daniel E L PromislowDepartment of Pathology, University of Washington, Seattle, WA, USA.
Matt KaeberleinDepartment of Pathology, University of Washington, Seattle, WA, USA.
Brian C KraemerDepartment of Pathology, University of Washington, Seattle, WA, USA.
Adrienne WangDepartment of Biology, Western Washington University, Bellingham, WA, USA.
Franco GuscettiInstitute of Veterinary Pathology, Vetsuisse Faculty, University of Zürich, Zürich, Switzerland.ORCID 0000-0002-3173-4811
Martin DarvasDepartment of Pathology, University of Washington, Seattle, WA, USA.

Funding

THERAPEUTIC EFFECTS OF INTRA-NASAL INSULIN DETEMIRP50AG005136 · NIA · UNIVERSITY OF WASHINGTON · PI BUCHWALD, DEDRA S · 1985 to 2019
$57.2M
The Dog Aging Project: Genetic and Environmental Determinants of Healthy Aging in Companion Dogs Competitive RevisionU19AG057377 · NIA · UNIVERSITY OF WASHINGTON · PI PROMISLOW, DANIEL EDWARD · 2018 to 2023
$29.0M
Developing Neuroprotective Strategies for Tau and TDP-43 Proteinopathy in FTLDR01NS064131 · NINDS · SEATTLE INST FOR BIOMEDICAL/CLINICAL RES · PI KRAEMER, BRIAN C. · 2009 to 2022
$5.0M
A systems biology approach in Drosophila to identify novel factors that influence AD pathogenicityRF1AG057330 · NIA · UNIVERSITY OF WASHINGTON · PI PROMISLOW, DANIEL EDWARD · 2017 to 2017
$3.4M
Conserved Mechanisms of Aging in Alzheimer DiseaseR21AG056872 · NIA · UNIVERSITY OF WASHINGTON · PI PROMISLOW, DANIEL EDWARD · 2017 to 2018
$426k
Inhibiting pathological TDP-43 phosphorylation as a therapeutic strategy for ALSI01BX003755 · VA · VA PUGET SOUND HEALTHCARE SYSTEM · PI KRAEMER, BRIAN C. · 2017 to 2020
–
BLRD VA I01 BX002619BLRD VA I01 BX003755NIA NIH HHS P50 AG005136NIA NIH HHS R21 AG056872NIA NIH HHS RF1 AG057330NIA NIH HHS U19 AG057377NINDS NIH HHS R01 NS064131
6 · The paper itself

Abstract

A major obstacle for preclinical testing of Alzheimer's disease (AD) therapies is the availability of translationally relevant AD models. Critical for the validation of such models is the application of the same approaches and techniques used for the neuropathological characterization of AD. Deposition of amyloid-β 42 (Aβ42) plaques and neurofibrillary tangles containing phospho-Tau (pTau) are the pathognomonic features of AD. In the neuropathologic evaluation of AD, immunohistochemistry (IHC) is the current standard method for detection of Aβ42 and pTau. Although IHC is indispensable for determining the distribution of AD pathology, it is of rather limited use for assessment of the quantity of AD pathology. We have recently developed Luminex-based assays for the quantitative assessment of Aβ42 and pTau in AD brains. These assays are based on the same antibodies that are used for the IHC-based diagnosis of AD neuropathologic change. Here we report the application and extension of such quantitative AD neuropathology assays to commonly used genetically engineered AD models and to animals that develop AD neuropathologic change as they age naturally. We believe that identifying AD models that have Aβ42 or pTau levels comparable to those observed in AD will greatly improve the ability to develop AD therapies.

Indexed as

Alzheimer’s diseaseamyloid β42cortexLuminexphospho-Tau

Identifiers

PMID31528297
PMCPMC6735310

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Registered trials

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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.