Evidence map›Paper›PMID 23036592›Full record

ArticleJournal of neuroimmunology2013

A peptide prime-DNA boost immunization protocol provides significant benefits as a new generation Aβ42 DNA vaccine for Alzheimer disease.

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

Abstract read
In one paragraph

Article in Journal of neuroimmunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed, 30 citations in OpenAlex.

  1. Vaccines for Alzheimer's disease: a brief scoping review.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Article
  2. Article
  3. Active full-length DNA AβAlzheimer's research & therapy · 2018
    Article
  4. Article
  5. Article
  6. Article
  7. DNA vaccines for prostate cancer.Pharmacology & therapeutics · 2017
    Review
  8. Article
  9. Review
  10. 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
  11. Review
  12. Article
  13. Article
  14. Review
  15. Alzheimer's disease: is a vaccine possible?Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2014
    Article
  16. Review
  17. Article
  18. 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 and Neurotherapeutics, University of Texas Southwestern Medical Center, Dallas, TX, United States. Doris.Lambracht-Washington@utsouthwestern.edu
Bao-xi Qu
Min Fu
Larry D Anderson
Todd N Eagar
Olaf Stüve
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 P30AG12300-17
6 · The paper itself

Abstract

Immunotherapy has the potential to provide a possible treatment therapy to prevent or delay Alzheimer disease. In a clinical trial (AN1792) in which patients received this immunotherapy and received active Aβ1-42 peptide immunizations, treatment was stopped when 6% of patients showed signs of meningoencephalitis. Follow up on these patients led to the conclusion that the antibody response was beneficial in removing Aβ1-42 from brain but an accompanying inflammatory Th1 T cell response was harmful. As a safe alternative treatment targeting the same self protein, Aβ1-42, in brain, we and others are working on a DNA Aβ1-42 immunization protocol as the immune response to DNA immunizations differs in many aspects from immunizations with peptide antigens. Because the immune response to DNA vaccination has different kinetics and has a significantly lower antibody production, we evaluated two different prime boost regimens, Aβ1-42 DNA prime/Aβ1-42 peptide boost and Aβ1-42 peptide prime/Aβ1-42 DNA boost for their effectiveness in antibody production and possible side effects due to inflammatory T cell responses. While both boost regimes significantly enhanced the specific antibody production with comparable antibody concentrations, the absence of the Aβ1-42 T cell response (no proliferation and no cytokine production) is consistent with our previous findings using this DNA Aβ1-42 trimer immunization and greatly enhances the safety aspect for possible clinical use.

Indexed as

Amyloid beta-PeptidesAnimalsAntibodiesAntibody FormationCell ProliferationCytokinesEnzyme-Linked Immunosorbent AssayEpitope MappingHumansMiceMice, Inbred StrainsPeptide FragmentsSpleenTh2 CellsT-LymphocytesVaccinationAmyloid beta-Peptidesamyloid beta-protein (1-42)AntibodiesCytokinesPeptide FragmentsVaccines, DNA

Identifiers

PMID23036592
PMCPMC4084825
OpenAlexW2095387508

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.