Evidence map›Paper›PMID 20149872›Full record

ArticleNeurobiology of disease2010

Triflusal reduces dense-core plaque load, associated axonal alterations and inflammatory changes, and rescues cognition in a transgenic mouse model of Alzheimer's disease.

M Coma, L Serenó, B Da Rocha-Souto, T C Scotton, J España, M B Sánchez, M Rodríguez, J Agulló, C Guardia-Laguarta, M Garcia-Alloza and 7 more

Open access · greenAbstract read
In one paragraph

Article in Neurobiology of disease, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
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  4. Review
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  7. Cyclooxygenase-2 Induced the β-Amyloid Protein Deposition and Neuronal Apoptosis Via Upregulating the Synthesis of Prostaglandin ENeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019
    Article
  8. The Role of Eicosanoids in Alzheimer's Disease.International journal of environmental research and public health · 2019
    Review
  9. Article
  10. Article
  11. Review
  12. Cyclooxygenase-1-dependent prostaglandins mediate susceptibility to systemic inflammation-induced acute cognitive dysfunction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  13. Article
  14. Inflammatory process in Alzheimer's Disease.Frontiers in integrative neuroscience · 2013
    Article
  15. Article
  16. Non-steroidal anti-inflammatory drugs and cognitive function: are prostaglandins at the heart of cognitive impairment in dementia and delirium?Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2012
    Review
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 4 institutions in 2 countries.

M ComaNeurology Department, Hospital de la Santa Creu i Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain.
L Serenó
B Da Rocha-Souto
T C Scotton
J España
M B Sánchez
M Rodríguez
J Agulló
C Guardia-Laguarta
M Garcia-Alloza
L A Borrelli
J Clarimón
A Lleó
B J Bacskai
C A Saura
B T Hyman
T Gómez-Isla
Harvard University · USHospital de Sant Pau · ESUniversitat Autònoma de Barcelona · ESMassachusetts General Hospital · US

Funding

THE ROLE OF ADVANCED CAA IN ALZHEIMER'S DEMENTIAP50AG005134 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI HYMAN, BRADLEY T. · 1985 to 2018
$42.1M
Research Education ComponentP30AG062421 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI Sudeshna Das · 2019 to 2026
$36.5M
Mechanisms of amyloid-beta clearance.R01AG020570 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI BACSKAI, BRIAN J · 2003 to 2006
$1.2M
Faculty recruitment for programs in the biology of age-related cognitive changeP30AG036449 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI HYMAN, BRADLEY T. · 2009 to 2010
$1.2M
NIA NIH HHS NIH AG020570NIA NIH HHS P30 AG036449NIA NIH HHS P30 AG062421NIA NIH HHS P50 AG005134NIA NIH HHS R01 AG020570
6 · The paper itself

Abstract

Inflammation has been associated with the two classic lesions in the Alzheimer's (AD) brain, amyloid deposits and neurofibrillary tangles. Recent data suggest that Triflusal, a compound with potent anti-inflammatory effects in the central nervous system in vivo, might delay the conversion from amnestic mild cognitive impairment to a fully established clinical picture of dementia. In the present study, we investigated the effect of Triflusal on brain Abeta accumulation, neuroinflammation, axonal curvature and cognition in an AD transgenic mouse model (Tg2576). Triflusal treatment did not alter the total brain Abeta accumulation but significantly reduced dense-cored plaque load and associated glial cell proliferation, proinflammatory cytokine levels and abnormal axonal curvature, and rescued cognitive deficits in Tg2576 mice. Behavioral benefit was found to involve increased expression of c-fos and BDNF, two of the genes regulated by CREB, as part of the signal transduction cascade underlying the molecular basis of long-term potentiation. These results add preclinical evidence of a potentially beneficial effect of Triflusal in AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsAxonsBrainBrain-Derived Neurotrophic FactorCentral Nervous System AgentsCognition DisordersCytokinesDisease Models, AnimalHumansMiceMice, Inbred C57BLMice, TransgenicNeurogliaPlaque, AmyloidAmyloid beta-PeptidesBrain-Derived Neurotrophic FactorCentral Nervous System AgentsCytokinesProto-Oncogene Proteins c-fosSalicylatestriflusal

Identifiers

PMID20149872
PMCPMC3707138
OpenAlexW2072227017

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.