Evidence map›Paper›PMID 25827781›Full record

ArticleNeurotoxicity research2015

Atorvastatin Prevents Cognitive Deficits Induced by Intracerebroventricular Amyloid-β1-40 Administration in Mice: Involvement of Glutamatergic and Antioxidant Systems.

Wagner C Martins, Vanessa Valgas dos Santos, Alessandra Antunes dos Santos, Samuel Vandresen-Filho, Tharine A Dal-Cim, Karen A de Oliveira, Claudia B N Mendes-de-Aguiar, Marcelo Farina, Rui Daniel Prediger, Giordano Gubert Viola and 1 more

Abstract read
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In one paragraph

Article in Neurotoxicity research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

14 citing papers in PubMed, 28 citations in OpenAlex.

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  11. Atorvastatin Protects from AβMolecular neurobiology · 2017
    Article
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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

11 authors at 3 institutions in 2 countries.

Wagner C MartinsDepartamento de Bioquímica, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, Trindade, Florianópolis, SC, 88040-900, Brazil.
Vanessa Valgas dos Santos
Alessandra Antunes dos Santos
Samuel Vandresen-Filho
Tharine A Dal-Cim
Karen A de Oliveira
Claudia B N Mendes-de-Aguiar
Marcelo Farina
Rui Daniel Prediger
Giordano Gubert Viola
Carla I Tasca
Universidade Federal de Santa Catarina · BRMonash University · AUUniversidade Federal de Sergipe · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Deposition of amyloid-β (Aβ) peptides into specific encephalic structures has been pointed as an important event related to Alzheimer's disease pathogenesis and associated with activation of glial cells, neuroinflammation, oxidative responses, and cognitive deficits. Aβ-induced pro-oxidative damage may regulate the activity of glutamate transporters, leading to reduced glutamate uptake and, as a consequence, excitotoxic events. Herein, we evaluated the effects of the pretreatment of atorvastatin, a HMG-CoA reductase inhibitor, on behavioral and biochemical alterations induced by a single intracerebroventricular (i.c.v.) injection of aggregated Aβ1-40 in mice. Atorvastatin (10 mg/kg/day, p.o.) was administered through seven consecutive days before Aβ1-40 administration. Aβ1-40 caused significant cognitive impairment in the object-place recognition task (2 weeks after the i.c.v. injection) and this phenomenon was abolished by atorvastatin pretreatment. Ex vivo evaluation of glutamate uptake into hippocampal and cerebral cortices slices showed atorvastatin, and Aβ1-40 decreased hippocampal and cortical Na(+)-dependent glutamate uptake. However, Aβ1-40 increased Na(+)-independent glutamate uptake and it was prevented by atorvastatin in prefrontal cortex slices. Moreover, Aβ1-40 treatment significantly increased the cerebrocortical activities of glutathione reductase and glutathione peroxidase and these events were blunted by atorvastatin pretreatment. Reduced or oxidized glutathione levels were not altered by Aβ1-40 and/or atorvastatin treatment. These results extend the notion of the protective action of atorvastatin against neuronal toxicity induced by Aβ1-40 demonstrating that a pretreatment with atorvastatin prevents the spatial learning and memory deficits induced by Aβ in rodents and promotes changes in glutamatergic and antioxidant systems mainly in prefrontal cortex.

Indexed as

AcetylcholinesteraseAmyloid beta-PeptidesAnimalsAtorvastatinCognition DisordersGlutamic AcidHippocampusHydroxymethylglutaryl-CoA Reductase InhibitorsInfusions, IntraventricularMaleMiceOxidative StressPeptide FragmentsPrefrontal CortexRecognition, PsychologySpatial LearningAcetylcholinesteraseAmyloid beta-Peptidesamyloid beta-protein (1-40)AtorvastatinGlutamic AcidHydroxymethylglutaryl-CoA Reductase InhibitorsPeptide Fragments

Identifiers

PMID25827781
OpenAlexW1981164333

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.