Evidence map›Paper›PMID 20471477›Full record

ReviewBiochimica et biophysica acta2010

Murine models of Alzheimer's disease and their use in developing immunotherapies.

Thomas Wisniewski, Einar M Sigurdsson

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Biochimica et biophysica acta, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

45 citing papers in PubMed, 81 citations in OpenAlex.

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  18. 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
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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 2 institutions 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
Einar M Sigurdsson
Neurology, Inc · USNew York University · US

Funding

PSYCHOSOCIAL COREP30AG008051 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SHAO, YONGZHAO · 1990 to 2019
$36.1M
Research Supplement to Promote Diversity in Health-Related ResearchR01AG032611 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI Einar M Sigurdsson · 2008 to 2026
$9.7M
Detection and Clearance of AD LesionsR01AG020245 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI WISNIEWSKI, THOMAS M · 2002 to 2016
$4.7M
Immune Therapy for AD plaques and Tangles in Tg MiceR01AG020197 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SIGURDSSON, EINAR M · 2001 to 2013
$2.8M
AMYLOID BETA PEPTIDE AND THEIR BINDING PROTEINSR01AG015408 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI WISNIEWSKI, THOMAS M · 1998 to 2009
$2.2M
Immunotherapy for Pancreatic Amylin Aggregates in DiabetesR21DK075494 · NIDDK · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SIGURDSSON, EINAR M · 2007 to 2008
$460k
NIA NIH HHS AG020197NIA NIH HHS AG032611NIA NIH HHS AG15408NIA NIH HHS AG20245NIA NIH HHS P30 AG008051NIA NIH HHS R01 AG015408NIA NIH HHS R01 AG020197NIA NIH HHS R01 AG020245NIA NIH HHS R01 AG032611NIDDK NIH HHS R21 DK075494
6 · The paper itself

Abstract

Alzheimer's disease (AD) is one of the categories of neurodegenerative diseases characterized by a 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 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. An additional important feature of AD is the accumulation of abnormally phosphorylated tau as soluble toxic oligomers and as neurofibrillary tangles. 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 specific aspects of AD pathology. None of the current murine models is a perfect match of the human disease. Perhaps the most exciting of the therapeutic approaches being developed is immunomodulation targeting the aggregating proteins, Abeta and tau. This type of AD therapy is currently being assessed in many transgenic mouse models, and promising findings have led to clinical trials. However, there is a discrepancy between results in murine models and ongoing clinical trials, which highlight the limitations of these models and also of our understanding of the underlying etiology and pathogenesis of AD. Because of these uncertainties, Tg models for AD are continuously being refined with the aim to better understand the disease and to enhance the predictive validity of potential treatments such as immunotherapies.

Indexed as

Disease Models, AnimalImmunotherapyAlzheimer DiseaseAlzheimer VaccinesAnimalsHumansMiceAlzheimer Vaccines

Identifiers

PMID20471477
PMCPMC2930136
OpenAlexW2041492570

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.