Evidence map›Paper›PMID 12122052›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002

Inflammation-dependent cerebral deposition of serum amyloid a protein in a mouse model of amyloidosis.

Jun-Tao Guo, Jin Yu, David Grass, Frederick C de Beer, Mark S Kindy

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 17% 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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 150 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Intracranial atherosclerotic disease and neurodegeneration: a narrative review and plausible mechanisms.Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association · 2024
    Review
  7. Review
  8. Correlation between obesity and AlzheimerZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024
    Review
  9. Review
  10. Review
  11. Variation of the 2D Pattern of Brain Proteins in Mice Infected withInternational journal of molecular sciences · 2024
    Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Stress Response Is the Main Trigger of Sporadic Amyloidoses.International journal of molecular sciences · 2021
    Review
  19. Review
  20. Review

7 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

5 authors at 1 institution in 1 country.

Jun-Tao GuoDepartment of Biochemistry, University of Kentucky, Lexington, Kentucky 40536, USA.
Jin Yu
David Grass
Frederick C de Beer
Mark S Kindy
Veterans Health Administration · US

Funding

Oxidized Lipoproteins in NeurodegenerationR01NS039588 · NINDS · UNIVERSITY OF KENTUCKY · PI KINDY, MARK S · 2001 to 2004
$1.2M
MECHANISMS OF HEAD TRAUMA INDUCED LUNG INJURYP01NS031220 · NINDS · UNIVERSITY OF KENTUCKY · PI KINDY, MARK S · 1994 to 1998
–
NIA NIH HHS AG12891NINDS NIH HHS NS31220NINDS NIH HHS NS39588NINDS NIH HHS R01 NS039588
6 · The paper itself

Abstract

The major pathological hallmark of amyloid diseases is the presence of extracellular amyloid deposits. Serum amyloid A (SAA) is an apolipoprotein primarily produced in the liver. Serum protein levels can increase one thousandfold after inflammation. SAA is the precursor to the amyloid A protein found in deposits of systemic amyloid A amyloid (AA or reactive amyloid) in both mouse and human. To study the factors necessary for cerebral amyloid formation, we have created a transgenic mouse that expresses the amyloidogenic mouse Saa1 protein in the brain. Using the synapsin promoter to drive expression of the Saa1 gene, the brains of transgenic mice expressed both RNA and protein. Under noninflammatory conditions, transgenic mice do not develop AA amyloid deposits in the brain; however, induction of a systemic acute-phase response in transgenic mice enhanced amyloid deposition. This deposition was preceded by an increase in cytokine levels in the brain, suggesting that systemic inflammation may be a contributing factor to the development of cerebral amyloid. The nonsteroidal anti-inflammatory agent indomethacin reduced inflammation and protected against the deposition of AA amyloid in the brain. These studies indicate that inflammation plays an important role in the process of amyloid deposition, and inhibition of inflammatory cascades may attenuate amyloidogenic processes, such as Alzheimer's disease.

Indexed as

Age FactorsAmyloidosisAnimalsAnti-Inflammatory Agents, Non-SteroidalBlotting, NorthernBrainCytokinesDisease Models, AnimalEncephalitisIndomethacinLipopolysaccharidesMiceMice, TransgenicOrgan SpecificityPromoter Regions, GeneticRNA, MessengerAnti-Inflammatory Agents, Non-SteroidalCytokinesIndomethacinLipopolysaccharidesRNA, MessengerSerum Amyloid A ProteinSynapsins

Identifiers

PMID12122052
PMCPMC6757908
OpenAlexW1885605401

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.