Evidence map›Paper›PMID 21625960›Full record

ArticleCellular and molecular neurobiology2011

DNA immunization against amyloid beta 42 has high potential as safe therapy for Alzheimer's disease as it diminishes antigen-specific Th1 and Th17 cell proliferation.

Doris Lambracht-Washington, Bao-Xi Qu, Min Fu, Larry D Anderson, Olaf Stüve, Todd N Eagar, Roger N Rosenberg

Abstract read
In one paragraph

Article in Cellular and molecular neurobiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

31 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Acquired immunity and Alzheimer's disease.Journal of biomedical research · 2022
    Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Active full-length DNA AβAlzheimer's research & therapy · 2018
    Article
  11. Article
  12. Imbalance of Circulating TFrontiers in immunology · 2018
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Immunotherapeutic Approaches Targeting Amyloid-β, α-Synuclein, and Tau for the Treatment of Neurodegenerative Disorders.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2016
    Review
  18. T Cells-Protective or Pathogenic in Alzheimer's Disease?Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2015
    Review
  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

7 authors at 2 institutions in 1 country.

Doris Lambracht-WashingtonDepartment of Neurology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9036, USA.
Bao-Xi Qu
Min Fu
Larry D Anderson
Olaf Stüve
Todd N Eagar
Roger N Rosenberg
The University of Texas Southwestern Medical Center · USDallas VA Medical Center · US

Funding

ROLE OF GLUTAMATE IN ALZHEIMER'S DISEASEP30AG012300 · NIA · UT SOUTHWESTERN MEDICAL CENTER · PI ROSENBERG, ROGER NEWMAN · 1994 to 2016
$26.6M
NIA NIH HHS P30 AG012300NIA NIH HHS P30AG12300-16
6 · The paper itself

Abstract

The pathogenesis of Alzheimer's disease (AD) has been strongly associated with the accumulation of amyloid beta (Aβ) peptides in brain, and immunotherapy targeting Aβ provides potential for AD prevention. A clinical trial in which AD patients were immunized with Aβ42 peptide was stopped when 6% of participants showed meningoencephalitis, apparently due to an inflammatory Th1 immune response. Previously, we and other have shown that Aβ42 DNA vaccination via gene gun generates a Th2 cellular immune response, which was shown by analyses of the respective antibody isotype profiles. We also determined that in vitro T cell proliferation in response to Aβ42 peptide re-stimulation was absent in DNA Aβ42 trimer-immunized mice when compared to Aβ42 peptide-immunized mice. To further characterize this observation prospectively and longitudinally, we analyzed the immune response in wild-type mice after vaccination with Aβ42 trimer DNA and Aβ42 peptide with Quil A adjuvant. Wild-type mice were immunized with short-term (1-3× vaccinations) or long-term (6× vacinations) immunization strategies. Antibody titers and isotype profiles of the Aβ42 specific antibodies, as well as cytokine profiles and cell proliferation studies from this longitudinal study were determined. Sufficient antibody titers to effectively reduce Aβ42, but an absent T cell proliferative response and no IFNγ or IL-17 secretion after Aβ42 DNA trimer immunization minimizes the risk of inflammatory activities of the immune system towards the self antigen Aβ42 in brain. Therefore, Aβ42 DNA trimer immunization has a high probability to be effective and safe to treat patients with early AD.

Indexed as

ImmunizationAlzheimer DiseaseAmyloid beta-PeptidesAnimalsCell ProliferationCytokinesDNAEnzyme-Linked Immunospot AssayEpitopesFluoresceinsImmunity, HumoralMiceSuccinimidesTh17 CellsTh1 Cells5-(6)-carboxyfluorescein diacetate succinimidyl esterAmyloid beta-PeptidesCytokinesDNAEpitopesFluoresceinsSuccinimides

Identifiers

PMID21625960
PMCPMC3349443
OpenAlexW2093172220

What OpenQuestion holds

Textmetadata
LicenceTDM
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.