Evidence map›Paper›PMID 25362040›Full record

SynthesisJournal of Alzheimer's disease : JAD2015

Systematic review of the relationship between amyloid-β levels and measures of transgenic mouse cognitive deficit in Alzheimer's disease.

Avery M Foley, Zeena M Ammar, Robert H Lee, Cassie S Mitchell

Abstract readSystematic Review
PubMed Full text at PMC Publisher
In one paragraph

Synthesis in Journal of Alzheimer's disease : JAD, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 3 pooled it
–field-weighted citation impact
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

41 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  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

4 authors.

Avery M FoleyDepartment of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA, USA.
Zeena M AmmarDepartment of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA, USA.
Robert H LeeDepartment of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA, USA.
Cassie S MitchellDepartment of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA, USA.

Funding

A New Approach to ALSK01NS069616 · NINDS · GEORGIA INSTITUTE OF TECHNOLOGY · PI MITCHELL, CASSIE S · 2011 to 2015
$641k
Identification of Amyotrophic Lateral Sclerosis Clinical PredictorsR21NS081426 · NINDS · GEORGIA INSTITUTE OF TECHNOLOGY · PI MITCHELL, CASSIE S · 2013 to 2014
$389k
NINDS NIH HHS K01 NS069616NINDS NIH HHS NS069616NINDS NIH HHS NS081426NINDS NIH HHS R21 NS081426
6 · The paper itself

Abstract

Amyloid-β (Aβ) is believed to directly affect memory and learning in Alzheimer's disease (AD). It is widely suggested that there is a relationship between Aβ40 and Aβ42 levels and cognitive performance. In order to explore the validity of this relationship, we performed a meta-analysis of 40 peer-reviewed, published AD transgenic mouse studies that quantitatively measured Aβ levels in brain tissue after assessing cognitive performance. We examined the relationship between Aβ levels (Aβ40, Aβ42, or the ratio of Aβ42 to Aβ40) and cognitive function as measured by escape latency times in the Morris water maze or exploratory preference percentage in the novel object recognition test. Our systematic review examined five mouse models (Tg2576, APP, PS1, 3xTg, APP(OSK)-Tg), gender, and age. The overall result revealed no statistically significant correlation between quantified Aβ levels and experimental measures of cognitive function. However, enough of the trends were of the same sign to suggest that there probably is a very weak qualitative trend visible only across many orders of magnitude. In summary, the results of the systematic review revealed that mice bred to show elevated levels of Aβ do not perform significantly worse in cognitive tests than mice that do not have elevated Aβ levels. Our results suggest two lines of inquiry: 1) Aβ is a biochemical "side effect" of the AD pathology; or 2) learning and memory deficits in AD are tied to the presence of qualitatively "high" levels of Aβ but are not quantitatively sensitive to the levels themselves.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsCognition DisordersDisease Models, AnimalGene Expression RegulationHumansMaze LearningMiceMice, TransgenicAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAmyloid-βcognitive deficitmemoryMorris water mazemouse modelnovel object recognitionTg2576

Identifiers

PMID25362040
PMCPMC4346318

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.