Evidence map›Paper›PMID 20101719›Full record

ReviewThe Mount Sinai journal of medicine, New York

Vaccination as a therapeutic approach to Alzheimer's disease.

Thomas Wisniewski, Allal Boutajangout

Open access · bronzeAbstract readReview
In one paragraph

Review in The Mount Sinai journal of medicine, New York. 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
3.9field-weighted citation impact, top 6% 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, 50 citations in OpenAlex.

  1. Review
  2. A Novel Aβ B-Cell Epitope Vaccine (rCV01) for Alzheimer's Disease Improved Synaptic and Cognitive Functions in 3 × Tg-AD Mice.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2016
    Article
  3. Article
  4. Review
  5. Review
  6. 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
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Could immunomodulation be used to prevent prion diseases?Expert review of anti-infective therapy · 2012
    Article
  17. Genomics of Dementia: APOE- and CYP2D6-Related Pharmacogenetics.International journal of Alzheimer's disease · 2012
    Article
  18. 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

2 authors at 1 institution in 1 country.

Thomas WisniewskiDepartment of Neurology, New York University School of Medicine, New York, NY, USA.
Allal Boutajangout
New York University · US

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
AMYLOID BETA PEPTIDE AND THEIR BINDING PROTEINSR01AG015408 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI WISNIEWSKI, THOMAS M · 1998 to 2009
$2.2M
NIA NIH HHS AG15408NIA NIH HHS AG20245NIA NIH HHS P30 AG008051NIA NIH HHS R01 AG015408NIA NIH HHS R01 AG020245
6 · The paper itself

Abstract

Alzheimer's disease is the most common cause of dementia worldwide. Alzheimer's disease is a member of a broad range of neurodegenerative diseases characterized pathologically by the conformational change of a normal protein into a pathological conformer with a high beta-sheet content that renders it neurotoxic. In the case of Alzheimer's disease, the normal soluble amyloid beta peptide is converted into oligomeric/fibrillar amyloid beta. The oligomeric forms of amyloid beta have been hypothesized to be the most toxic, whereas fibrillar amyloid beta becomes deposited as amyloid plaques and congophilic angiopathy, which both serve as neuropathological markers of the disease. In addition, the accumulation of abnormally phosphorylated tau as soluble toxic oligomers and as neurofibrillary tangles is a critical part of the pathology. Numerous therapeutic interventions are under investigation to prevent and treat Alzheimer's disease. Among the most exciting and advanced of these approaches is vaccination. Immunomodulation is being tried for a range of neurodegenerative disorders, with great success being reported in most model animal trials; however, the much more limited human data have shown more modest clinical success so far, with encephalitis occurring in a minority of patients treated with active immunization. The immunomodulatory approaches for neurodegenerative diseases involve targeting a self-protein, albeit in an abnormal conformation; hence, effective enhanced clearance of the disease-associated conformer has to be balanced with the potential risk of stimulating excessive toxic inflammation within the central nervous system. The design of future immunomodulatory approaches that are more focused is dependent on addressing a number of questions, including when is the best time to start immunization, what are the most appropriate targets for vaccination, and is amyloid central to the pathogenesis of Alzheimer's disease or is it critical to target tau-related pathology also. In this review, we discuss the past experience with vaccination for Alzheimer's disease and the development of possible future strategies that target both amyloid beta-related and tau-related pathologies.

Indexed as

VaccinationAlzheimer DiseaseAmyloid beta-PeptidesAnimalsAntibodies, MonoclonalDisease Models, AnimalHumansMiceMice, Transgenictau ProteinsAmyloid beta-PeptidesAntibodies, Monoclonaltau Proteins

Identifiers

PMID20101719
PMCPMC3026780
OpenAlexW2031361708

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.