Evidence map›Paper›PMID 20101721›Full record

ReviewThe Mount Sinai journal of medicine, New York

Transgenic mouse models of Alzheimer's disease.

Gregory A Elder, Miguel A Gama Sosa, Rita De Gasperi

Open access · greenAbstract 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 153 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
153citing papers in PubMed, 3 pooled it
7.5field-weighted citation impact, top 2% 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

153 citing papers in PubMed, 3 syntheses or guidelines pooled it, 339 citations in OpenAlex.

  1. Pooled it
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  14. Research on Alzheimer's Disease (AD) Involving the Use ofCentral nervous system agents in medicinal chemistry · 2025
    Review
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93 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Gregory A ElderNeurology Service, James J. Peters Department of Veterans Affairs Medical Center, Bronx, NY, USA. gregory.elder@mssm.edu
Miguel A Gama Sosa
Rita De Gasperi
Icahn School of Medicine at Mount Sinai · USJames J. Peters VA Medical Center · US

Funding

VESICULAR LOCALIZATION AND FUNCTION OF PRESENILIN 1 FRAGMENTP50AG005138 · NIA · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI SCHIMMING, CORBETT · 1985 to 2019
$37.9M
QUANTITATIVE ANALYSIS OF MICROVASCULAR CHANGES IN THE AGING BRAINP01AG002219 · NIA · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI HAROUTUNIAN, VAHRAM · 1985 to 2009
$19.2M
Role of Presenilin-1 in Neural Injury and RepairR01AG020139 · NIA · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI ELDER, GREGORY A · 2002 to 2005
$1.0M
Presenilin-1 as an Hypoxia SensorR21AG029361 · NIA · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI ELDER, GREGORY A. · 2007 to 2008
$286k
Mechanisms Underlying the Vascular Pathology of Alzheimer's DiseaseI01BX000342 · VA · JAMES J PETERS VA MEDICAL CENTER · PI ELDER, GREGORY A. · 2009 to 2012
–
BLRD VA I01 BX000342NIA NIH HHS AG02219NIA NIH HHS AG029361NIA NIH HHS AG05138NIA NIH HHS AG20139NIA NIH HHS P01 AG002219NIA NIH HHS P50 AG005138NIA NIH HHS R01 AG020139NIA NIH HHS R21 AG029361
6 · The paper itself

Abstract

Alzheimer's disease is the most common cause of senile dementia in the United States and Europe. At present, there is no effective treatment. Given the disease's prevalence and poor prognosis, the development of animal models has been a high research priority. Transgenic modeling has been pursued on the basis of the amyloid hypothesis and has taken advantage of mutations in the amyloid precursor protein and the presenilins that cause familial forms of Alzheimer's disease. Modeling has been most aggressively pursued in mice, for which the techniques of genetic modification are well developed. Transgenic mouse models now exist that mimic a range of Alzheimer's disease-related pathologies. Although none of the models fully replicates the human disease, the models have contributed significant insights into the pathophysiology of beta-amyloid toxicity, particularly with respect to the effects of different beta-amyloid species and the possible pathogenic role of beta-amyloid oligomers. They have also been widely used in the preclinical testing of potential therapeutic modalities and have played a pivotal role in the development of immunotherapies for Alzheimer's disease that are currently in clinical trials. These models will, without a doubt, continue to play central roles in preclinical testing and be used as tools for developing insights into the biological basis of Alzheimer's disease.

Indexed as

Disease Models, AnimalMice, TransgenicAlzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsHumansMiceMutationPresenilinsAmyloid beta-Protein PrecursorPresenilins

Identifiers

PMID20101721
PMCPMC2925685
OpenAlexW2098977708

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.