Evidence map›Paper›PMID 27142962›Full record

ArticleScientific reports2016

Neuroprotective effects of the anticancer drug NVP-BEZ235 (dactolisib) on amyloid-β 1-42 induced neurotoxicity and memory impairment.

Paula Maria Quaglio Bellozi, Isabel Vieira de Assis Lima, Juliana Guimarães Dória, Érica Leandro Marciano Vieira, Alline Cristina Campos, Eduardo Candelario-Jalil, Helton José Reis, Antônio Lúcio Teixeira, Fabíola Mara Ribeiro, Antônio Carlos Pinheiro de Oliveira

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
3.5field-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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

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  5. Cognitive Impairment in Multiple Sclerosis.Bioengineering (Basel, Switzerland) · 2023
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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

10 authors at 3 institutions in 2 countries.

Paula Maria Quaglio BelloziDepartment of Pharmacology, Universidade Federal de Minas Gerais, Belo Horizonte, 31270-901, Brazil.
Isabel Vieira de Assis LimaDepartment of Pharmacology, Universidade Federal de Minas Gerais, Belo Horizonte, 31270-901, Brazil.
Juliana Guimarães DóriaDepartment of Biochemistry and Immunology, Universidade Federal de Minas Gerais, Belo Horizonte, 31270-901, Brazil.
Érica Leandro Marciano VieiraDepartment of Internal Medicine, Universidade Federal de Minas Gerais, Belo Horizonte, 30130-100, Brazil.
Alline Cristina CamposDepartment of Pharmacology, Universidade de São Paulo, Ribeirão Preto, 14049-900, Brazil.
Eduardo Candelario-JalilDepartment of Neuroscience, University of Florida, Gainesville, FL 32610, USA.
Helton José ReisDepartment of Pharmacology, Universidade Federal de Minas Gerais, Belo Horizonte, 31270-901, Brazil.
Antônio Lúcio TeixeiraDepartment of Internal Medicine, Universidade Federal de Minas Gerais, Belo Horizonte, 30130-100, Brazil.
Fabíola Mara RibeiroDepartment of Biochemistry and Immunology, Universidade Federal de Minas Gerais, Belo Horizonte, 31270-901, Brazil.
Antônio Carlos Pinheiro de OliveiraDepartment of Pharmacology, Universidade Federal de Minas Gerais, Belo Horizonte, 31270-901, Brazil.
Universidade Federal de Minas Gerais · BRUniversidade de Ribeirão Preto · BRUniversity of Florida · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's Disease (AD) is a progressive neurodegenerative disease and the main cause of dementia. Substantial evidences indicate that there is over-activation of the PI3K/Akt/mTOR axis in AD. Therefore, the aim of the present study was to investigate the effects of NVP-BEZ235 (BEZ; dactolisib), a dual PI3K/mTOR inhibitor that is under phase I/II clinical trials for the treatment of some types of cancer, in hippocampal neuronal cultures stimulated with amyloid-β (Aβ) 1-42 and in mice injected with Aβ 1-42 in the hippocampus. In cell cultures, BEZ reduced neuronal death induced by Aβ. BEZ, but not rapamycin, a mTOR inhibitor, or LY294002, a PI3K inhibitor that also inhibits mTOR, reduced the memory impairment induced by Aβ. The effect induced by Aβ was also prevented in PI3Kγ(-/-) mice. Neuronal death and microgliosis induced by Aβ were reduced by BEZ. In addition, the compound increased IL-10 and TNF-α levels in the hippocampus. Finally, BEZ did not change the phosphorylation of Akt and p70s6K, suggesting that the involvement of PI3K and mTOR in the effects induced by BEZ remains controversial. Therefore, BEZ represents a potential strategy to prevent the pathological outcomes induced by Aβ and should be investigated in other models of neurodegenerative conditions.

Indexed as

Amyloid beta-PeptidesAnimalsCells, CulturedCell SurvivalHippocampusImidazolesMemory DisordersMiceNeuronsNeuroprotective AgentsQuinolinesAmyloid beta-PeptidesdactolisibImidazolesNeuroprotective AgentsQuinolines

Identifiers

PMID27142962
PMCPMC4855228
OpenAlexW2347162009

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.