Evidence map›Paper›PMID 24330773›Full record

ArticleJournal of neuroinflammation2013

Immunomodulation targeting of both Aβ and tau pathological conformers ameliorates Alzheimer's disease pathology in TgSwDI and 3xTg mouse models.

Fernando Goñi, Krystal Herline, Daniel Peyser, Kinlung Wong, Yong Ji, Yanjie Sun, Pankaj Mehta, Thomas Wisniewski

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.5field-weighted citation impact, top 11% 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, 43 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Current and Future Treatments in Alzheimer Disease: An Update.Journal of central nervous system disease · 2020
    Review
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  6. Article
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  15. Article
  16. Article
  17. Review
  18. Chemical Fluorescent Probe for Detection of Aβ Oligomers.Journal of the American Chemical Society · 2015
    Article
  19. Review
  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

8 authors at 2 institutions in 2 countries.

Fernando Goñi
Krystal Herline
Daniel Peyser
Kinlung Wong
Yong Ji
Yanjie Sun
Pankaj Mehta
Thomas WisniewskiDepartment of Neurology, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA. Thomas.wisniewski@nyumc.org.
New York University · USTianjin Huanhu Hospital · CN

Funding

PSYCHOSOCIAL COREP30AG008051 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SHAO, YONGZHAO · 1990 to 2019
$36.1M
Detection and Clearance of AD LesionsR01AG020245 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI WISNIEWSKI, THOMAS M · 2002 to 2016
$4.7M
Therapeutic Targeting of Abnormal Conformation in Neurodegenerative DiseaseR01NS073502 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI WISNIEWSKI, THOMAS M · 2010 to 2019
$3.7M
NIA NIH HHS AG08051NIA NIH HHS AG20245NIA NIH HHS P30 AG008051NINDS NIH HHS NS073502NINDS NIH HHS R01 NS073502
6 · The paper itself

Abstract

backgroundCentral to the pathogenesis of Alzheimer's disease (AD) and many other neurodegenerative diseases is the conformational change of a normal self-protein into toxic oligomeric species and amyloid deposits. None of these disorders have an effective therapy, but immunization approaches hold great promise. We have previously shown that active immunization with a novel peptide when polymerized into a stable oligomeric conformation, pBri, induced a humoral immune response to toxic Aβ species in an AD model, APP/PS1 transgenic (Tg) mice, reducing plaque deposits. pBri is a glutaraldehyde polymerized form of the carboxyl fragment of an amyloidogenic protein, which is deposited in the brains of patients with a rare autosomal dominant disease due to a missense mutation in a stop codon, resulting in the translation of an intronic sequence, with no known sequence homology to any mammalian protein.

methodsIn the current study we tested whether pBri-peptide-based immunomodulation is effective at reducing both vascular amyloid deposits and tau-related pathology using TgSwDI mice with extensive congophilic angiopathy and 3xTg mice with tau pathology.

resultsOur results indicate that this immunomodulation approach, which produces a humoral response to proteins in a pathological conformation, is effective at reducing both Aβ and tau-related pathologies.

conclusionsThis immunomodulatory approach has the advantage of using a non-self-immunogen that is less likely to be associated with autoimmune toxicity. Furthermore we found that it is able to target all the cardinal features of AD concurrently.

Indexed as

ImmunizationAlzheimer DiseaseAmyloid beta-PeptidesAmyloidogenic ProteinsAnimalsBlotting, WesternDisease Models, AnimalEnzyme-Linked Immunosorbent AssayHumansLuminescent MeasurementsMiceMice, TransgenicMolecular MimicryProtein Structure, Secondarytau ProteinsAmyloid beta-PeptidesAmyloidogenic Proteinstau Proteins

Identifiers

PMID24330773
PMCPMC3878790
OpenAlexW2001271051

What OpenQuestion holds

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LicenceCC BY
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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.