Evidence map›Paper›PMID 21490226›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011

Naturally occurring autoantibodies against beta-amyloid: investigating their role in transgenic animal and in vitro models of Alzheimer's disease.

Richard Dodel, Karthikeyan Balakrishnan, Kathy Keyvani, Oliver Deuster, Frauke Neff, Luminita-Cornelia Andrei-Selmer, Stephan Röskam, Carsten Stüer, Yousef Al-Abed, Carmen Noelker and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
7.1field-weighted citation impact, top 2% 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

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 121 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Genetic evidence suggests a protective role of immunoglobulin M in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. TDP-43-specific Autoantibody Decline in Patients With Amyotrophic Lateral Sclerosis.Neurology(R) neuroimmunology & neuroinflammation · 2021
    Article
  13. Article
  14. Review
  15. Article
  16. Rationale for the development of an Alzheimer's disease vaccine.Human vaccines & immunotherapeutics · 2020
    Article
  17. Review
  18. Article
  19. Article
  20. Article

6 more citing papers are in PubMed but not listed here.

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

14 authors at 5 institutions in 2 countries.

Richard DodelDepartment of Neurology, Philipps University Marburg, D-35043 Marburg, Germany. dodel@med.uni-marburg.de
Karthikeyan Balakrishnan
Kathy Keyvani
Oliver Deuster
Frauke Neff
Luminita-Cornelia Andrei-Selmer
Stephan Röskam
Carsten Stüer
Yousef Al-Abed
Carmen Noelker
Monika Balzer-Geldsetzer
Wolfgang Oertel
Yansheng Du
Michael Bacher
Philipps University of Marburg · DEIndiana University – Purdue University Indianapolis · USNorthwell Health · USTechnical University of Munich · DEUniversity of Duisburg-Essen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder primarily affecting regions of the brain responsible for higher cognitive functions. Immunization against β-amyloid (Aβ) in animal models of AD has been shown to be effective on the molecular level but also on the behavioral level. Recently, we reported naturally occurring autoantibodies against Aβ (NAbs-Aβ) being reduced in Alzheimer's disease patients. Here, we further investigated their physiological role: in epitope mapping studies, NAbs-Aβ recognized the mid-/C-terminal end of Aβ and preferentially bound to oligomers but failed to bind to monomers/fibrils. NAbs-Aβ were able to interfere with Aβ peptide toxicity, but NAbs-Aβ did not readily clear senile plaques although early fleecy-like plaques were reduced. Administration of NAbs-Aβ in transgenic mice improved the object location memory significantly, almost reaching performance levels of wild-type control mice. These findings suggest a novel physiological mechanism involving NAbs-Aβ to dispose of proteins or peptides that are prone to forming toxic aggregates.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsAnimals, Genetically ModifiedAntibody FormationAutoantibodiesBehavior, AnimalBrainCells, CulturedChromatography, GelDisease Models, AnimalEpitopesFemaleHumansImmunizationImmunoglobulin GAmyloid beta-PeptidesAutoantibodiesEpitopesImmunoglobulin G

Identifiers

PMID21490226
PMCPMC6622820
OpenAlexW2083882468

What OpenQuestion holds

Textmetadata
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.