Evidence map›Paper›PMID 18571864›Full record

ArticleNeuroscience2008

Corticosterone and related receptor expression are associated with increased beta-amyloid plaques in isolated Tg2576 mice.

H Dong, C M Yuede, H-S Yoo, M V Martin, C Deal, A G Mace, J G Csernansky

Open access · greenAbstract read
In one paragraph

Article in Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 13% 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

64 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Experimental laboratory models as tools for understanding modifiable dementia risk.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. Metabolic disorder in Alzheimer's disease.Metabolic brain disease · 2021
    Review

4 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

7 authors at 1 institution in 1 country.

H DongDepartment of Psychiatry, Washington University School of Medicine, St Louis, MO 63110, USA. dongh@wustl.edu <dongh@wustl.edu>
C M Yuede
H-S Yoo
M V Martin
C Deal
A G Mace
J G Csernansky
Washington University in St. Louis · US

Funding

Stress, Glucocorticoids and Alzheimer DiseaseR01AG025824 · NIA · WASHINGTON UNIVERSITY · PI CSERNANSKY, JOHN G · 2005 to 2009
$1.6M
NIA NIH HHS AG 025824NIA NIH HHS R01 AG025824
6 · The paper itself

Abstract

Previously, we reported that the stress associated with chronic isolation was associated with increased beta-amyloid (Abeta) plaque deposition and memory deficits in the Tg2576 transgenic animal model of Alzheimer's disease (AD) [Dong H, Goico B, Martin M, Csernansky CA, Bertchume A, Csernansky JG (2004) Effects of isolation stress on hippocampal neurogenesis, memory, and amyloid plaque deposition in APP (Tg2576) mutant mice. Neuroscience 127:601-609]. In this study, we investigated the potential mechanisms of stress-accelerated Abeta plaque deposition in this Tg2576 mice by examining the relationship between plasma corticosterone levels, expression of glucocorticoid receptor (GR) and corticotropin-releasing factor receptor-1 (CRFR1) in the brain, brain tissue Abeta levels and Abeta plaque deposition during isolation or group housing from weaning (i.e. 3 weeks of age) until 27 weeks of age. We found that isolation housing significantly increased plasma corticosterone levels as compared with group-housing in both Tg+ mice (which contain and overexpress human amyloid precursor protein (hAPP) gene) and Tg- mice (which do not contain hAPP gene as control). Also, isolated, but not group-housed animals showed increases in the expression of GR in the cortex. Furthermore, the expression of CRFR1 was increased in isolated Tg+ mice, but decreased in isolated Tg- mice in both cortex and hippocampus. Changes in the components of hypothalamic-pituitary-adrenal (HPA) axis were accompanied by increases in brain tissue Abeta levels and Abeta plaque deposition in the hippocampus and overlying cortex in isolated Tg+ mice. These results suggest that isolation stress increases corticosterone levels and GR and CRFR1 expression in conjunction with increases in brain tissue Abeta levels and Abeta plaque deposition in the Tg2576 mouse model of AD.

Indexed as

Amyloid beta-PeptidesAmyloid beta-Protein PrecursorAnalysis of VarianceAnimalsBenzothiazolesCorticosteroneCRF Receptor, Type 1Disease Models, AnimalHippocampusHumansMiceMice, TransgenicMutationPlaque, AmyloidReceptors, Corticotropin-Releasing HormoneReceptors, GlucocorticoidAmyloid beta-PeptidesAmyloid beta-Protein PrecursorBenzothiazolesCorticosteroneCRF Receptor, Type 1Receptors, Corticotropin-Releasing HormoneReceptors, GlucocorticoidThiazolesthioflavin T

Identifiers

PMID18571864
PMCPMC2664643
OpenAlexW2066497382

What OpenQuestion holds

Textmetadata
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.