Evidence map›Paper›PMID 15052274›Full record

ReviewMolecular psychiatry2004

Transgenic animal models of Alzheimer's disease and related disorders: histopathology, behavior and therapy.

J Götz, J R Streffer, D David, A Schild, F Hoerndli, L Pennanen, P Kurosinski, F Chen

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Molecular psychiatry, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05601856 (Gut Microbiome and Blood Indices in Patients With AD and Their Spousal Caregivers), which is not on this map. Cited by 111 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed, 2 pooled it
11.3field-weighted citation impact, top 1% 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.

NCT05601856 unknown statusnot on this mapstarted 2022, after this paper: background citation

Gut Microbiome and Blood Indices in Patients With AD and Their Spousal Caregivers

TypeobservationalSponsorUniversity of VirginiaRan2022 to 2025Enrolled104ConditionsAlzheimer Disease, Gut Biome
3 · Its place in the literature

Who cites it

111 citing papers in PubMed, 2 syntheses or guidelines pooled it, 273 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
  6. Experimental modeling of Alzheimer's disease: Translational lessons from cross-taxon analyses.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Plasma βAlzheimer's research & therapy · 2023
    Article
  16. Review
  17. Review
  18. Amyloid Beta in Aging and Alzheimer's Disease.International journal of molecular sciences · 2022
    Review
  19. Protective effects ofNutrition research and practice · 2022
    Article
  20. Review

51 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

8 authors at 1 institution in 1 country.

J GötzDivision of Psychiatry Research, University of Zürich, August Forel Str. 1, CH-8008 Zürich, Switzerland. goetz@bli.unizh.ch
J R Streffer
D David
A Schild
F Hoerndli
L Pennanen
P Kurosinski
F Chen
University of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a devastating neurodegenerative disease that affects more than 15 million people worldwide. Within the next generation, these numbers will more than double. To assist in the elucidation of pathogenic mechanisms of AD and related disorders, such as frontotemporal dementia (FTDP-17), genetically modified mice, flies, fish and worms were developed, which reproduce aspects of the human histopathology, such as beta-amyloid-containing plaques and tau-containing neurofibrillary tangles (NFT). In mice, the tau pathology caused selective behavioral impairment, depending on the distribution of the tau aggregates in the brain. Beta-amyloid induced an increase in the numbers of NFT, whereas the opposite was not observed in mice. In beta-amyloid-producing transgenic mice, memory impairment was associated with increased levels of beta-amyloid. Active and passive beta-amyloid-directed immunization caused the removal of beta-amyloid plaques and restored memory functions. These findings have since been translated to human therapy. This review aims to discuss the suitability and limitations of the various animal models and their contribution to an understanding of the pathophysiology of AD and related disorders.

Indexed as

Alzheimer DiseaseDisease Models, AnimalMice, TransgenicAnimalsDrosophilaHumansMice

Identifiers

PMID15052274
OpenAlexW1989146486

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.