Evidence map›Paper›PMID 22167652›Full record

ArticleNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2012

Effects of chronic guanosine treatment on hippocampal damage and cognitive impairment of rats submitted to chronic cerebral hypoperfusion.

Marcelo Ganzella, Enderson Dias Alves de Oliveira, Daniel Diniz Comassetto, Fernanda Cechetti, Victor Hermes Cereser, Júlia Dubois Moreira, Gisele Hansel, Roberto Farina Almeida, Denise Barbosa Ramos, Yanier Nuñes Figueredo and 6 more

Abstract read
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In one paragraph

Article in Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

25 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
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  3. Article
  4. Review
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  7. Review
  8. Article
  9. Article
  10. Article
  11. Adenosine ACells · 2019
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Guanosine and its role in neuropathologies.Purinergic signalling · 2016
    Review
  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

16 authors at 3 institutions in 3 countries.

Marcelo GanzellaDepartamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Ramiro Barcellos, 2600, anexo, Santana, Porto Alegre, RS 90035-003, Brazil. ganzellam@hotmail.com
Enderson Dias Alves de Oliveira
Daniel Diniz Comassetto
Fernanda Cechetti
Victor Hermes Cereser
Júlia Dubois Moreira
Gisele Hansel
Roberto Farina Almeida
Denise Barbosa Ramos
Yanier Nuñes Figueredo
Debora Guerini Souza
Jean Pierre Oses
Paulo Valdeci Worm
Matilde Achaval
Carlos Alexandre Netto
Diogo Onofre Souza
Universidade Federal do Rio Grande do Sul · BRCentro de Investigación y Desarrollo de medicamentosUniversidade Católica de Pelotas · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic cerebral hypoperfusion contributes to a cognitive decline related to brain disorders. Its experimental model in rats is a permanent bilateral common carotid artery occlusion (2VO). Overstimulation of the glutamatergic system excitotoxicity due to brain energetic disturbance in 2VO animals seems to play a pivotal role as a mechanism of cerebral damage. The nucleoside guanosine (GUO) exerts extracellular effects including antagonism of glutamatergic activity. Accordingly, our group demonstrated several neuroprotective effects of GUO against glutamatergic excitotoxicity. Therefore, in this study, we evaluated a chronic GUO treatment effects in rats submitted to 2VO. We evaluated the animals performance in the Morris water maze and hippocampal damage by neurons and astrocytes immunohistochemistry. In addition, we investigated the cerebrospinal fluid (CSF) brain derived neurotrophic factor (BDNF) and serum S100B levels. Additionally, the purine CSF and plasma levels were determined. GUO treatment did not prevent the cognitive impairment promoted by 2VO. However, none of the 2VO animals treated with GUO showed differences in the hippocampal regions compared to control, while 20% of 2VO rats not treated with GUO presented loss of pyramidal neurons and increased glial labeling cells in CA1 hippocampal region. In addition, we did not observe differences in CSF BDNF nor serum S100B levels among the groups. Of note, both the 2VO surgery and GUO treatment changed the purine CSF and plasma profile. In conclusion, GUO treatment did not prevent the cognitive impairment observed in 2VO animals, but our data suggest that GUO could be neuroprotective against hippocampal damage induced by 2VO.

Indexed as

AnimalsBrain IschemiaChromatography, High Pressure LiquidCognitionCognition DisordersGuanosineHippocampusImmunohistochemistryMaleMaze LearningNeuroprotective AgentsPurinesRatsRats, WistarGuanosineNeuroprotective AgentsPurines

Identifiers

PMID22167652
OpenAlexW2014983500

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.