Evidence map›Paper›PMID 20012091›Full record

ReviewBrain structure & function2010

Immunotherapeutic approaches for Alzheimer's disease in transgenic mouse models.

Thomas Wisniewski, Allal Boutajangout

Abstract readReview
In one paragraph

Review in Brain structure & function, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. 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
  5. Article
  6. Article
  7. Tau-Directed Immunotherapy: A Promising Strategy for Treating Alzheimer's Disease and Other Tauopathies.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2016
    Review
  8. Article
  9. Immunotherapy for Alzheimer's disease.Biochemical pharmacology · 2014
    Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Could immunomodulation be used to prevent prion diseases?Expert review of anti-infective therapy · 2012
    Article
  15. Review
  16. Article
  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

2 authors at 1 institution in 1 country.

Thomas WisniewskiDepartment of Neurology, New York University School of Medicine, 550 First Avenue, New York, NY, 10016, USA. thomas.wisniewski@nyumc.org
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
Therapeutic Targeting of Abnormal Conformation in Neurodegenerative DiseaseR01NS073502 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI WISNIEWSKI, THOMAS M · 2010 to 2019
$3.7M
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 AG020245NINDS NIH HHS R01 NS073502
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a member of a category of neurodegenerative diseases characterized by the conformational change of a normal protein into a pathological conformer with a high beta-sheet content that renders it resistant to degradation and neurotoxic. In the case of AD the normal soluble amyloid beta (sAbeta) peptide is converted into oligomeric/fibrillar Abeta. The oligomeric forms of Abeta are thought to be the most toxic, while fibrillar Abeta 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 an essential part of the pathology. Many therapeutic interventions are under investigation to prevent and treat AD. The testing of these diverse approaches to ameliorate AD pathology has been made possible by the existence of numerous transgenic mouse models which each mirror different aspects of AD pathology. Perhaps the most exciting of these approaches is immunomodulation. Vaccination is currently being tried for a range of age associated CNS disorders with great success being reported in many transgenic mouse models. However, there is a discrepancy between these results and current human clinical trials which highlights the limitations of current models and also uncertainties in our understanding of the underlying pathogenesis of AD. No current AD Tg mouse model exactly reflects all aspects of the human disease. Since the underlying etiology of sporadic AD is unknown, the process of creating better Tg models is in constant evolution. This is an essential goal since it will be necessary to develop therapeutic approaches which will be highly effective in humans.

Indexed as

Alzheimer DiseaseAlzheimer VaccinesAmyloid beta-PeptidesAnimalsCerebral Amyloid AngiopathyDisease Models, AnimalImmunomodulationImmunotherapyMiceMice, TransgenicPlaque, Amyloidtau ProteinsAlzheimer VaccinesAmyloid beta-Peptidestau Proteins

Identifiers

PMID20012091
PMCPMC3124148
OpenAlexW2001723966

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.