Evidence map›Paper›PMID 27155503›Full record

SynthesisBehavioural brain research2017

Transcriptional signatures of brain aging and Alzheimer's disease: What are our rodent models telling us?

Kendra E Hargis, Eric M Blalock

Open access · hybridAbstract readMeta-Analysis
In one paragraph

Synthesis in Behavioural brain research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
6.4field-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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Nontransgenic Guinea Pig Strains Exhibit Hallmarks of Human Brain Aging and Alzheimer's Disease.The journals of gerontology. Series A, Biological sciences and medical sciences · 2022
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Genetic architecture of Alzheimer's disease.Neurobiology of disease · 2020
    Review
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.

Kendra E HargisUniversity of Kentucky College of Medicine, Department of Pharmacology and Nutritional Science, Lexington, KY, United States.
Eric M BlalockUniversity of Kentucky College of Medicine, Department of Pharmacology and Nutritional Science, Lexington, KY, United States. Electronic address: emblal@uky.edu.
University of Kentucky · US

Funding

Psychosocial stress interactions with electrophysiology and brain agingR01AG037868 · NIA · UNIVERSITY OF KENTUCKY · PI BLALOCK, ERIC · 2011 to 2025
$3.5M
Hippocampal Electrophysiology and Myelinogenesis in Healthy Cognitive AgingR01AG034605 · NIA · UNIVERSITY OF KENTUCKY · PI LANDFIELD, PHILIP W. · 2009 to 2015
$2.9M
TRAINING PROGRAM IN OXIDATIVE STRESS AND NUTRITIONT32DK007778 · NIDDK · UNIVERSITY OF KENTUCKY · PI WEBB, NANCY R · 2000 to 2019
$2.5M
NIA NIH HHS R01 AG034605NIA NIH HHS R01 AG037868NIDDK NIH HHS T32 DK007778
6 · The paper itself

Abstract

Aging is the biggest risk factor for idiopathic Alzheimer's disease (AD). Recently, the National Institutes of Health released AD research recommendations that include: appreciating normal brain aging, expanding data-driven research, using open-access resources, and evaluating experimental reproducibility. Transcriptome data sets for aging and AD in humans and animal models are available in NIH-curated, publically accessible databases. However, little work has been done to test for concordance among those molecular signatures. Here, we test the hypothesis that brain transcriptional profiles from animal models recapitulate those observed in the human condition. Raw transcriptional profile data from twenty-nine studies were analyzed to produce p-values and fold changes for young vs. aged or control vs. AD conditions. Concordance across profiles was assessed at three levels: (1) # of significant genes observed vs. # expected by chance; (2) proportion of significant genes showing directional agreement; (3) correlation among studies for magnitude of effect among significant genes. The highest concordance was found within subjects across brain regions. Normal brain aging was concordant across studies, brain regions, and species, despite profound differences in chronological aging among humans, rats and mice. Human studies of idiopathic AD were concordant across brain structures and studies, but were not concordant with the transcriptional profiles of transgenic AD mouse models. Further, the five transgenic AD mouse models that were assessed were not concordant with one another. These results suggest that normal brain aging is similar in humans and research animals, and that different transgenic AD model mice may reflect selected aspects of AD pathology.

Indexed as

TranscriptomeAgingAlzheimer DiseaseAnimalsDisease Models, AnimalGene Expression ProfilingHumansMiceRatsSpecies SpecificityAgingAlzheimer’s diseaseTranscriptome

Identifiers

PMID27155503
PMCPMC5533609
OpenAlexW2346448457

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.