Evidence map›Paper›PMID 28243355›Full record

ArticleOxidative medicine and cellular longevity2017

Age and Environment Influences on Mouse Prion Disease Progression: Behavioral Changes and Morphometry and Stereology of Hippocampal Astrocytes.

J Bento-Torres, L L Sobral, R R Reis, R B de Oliveira, D C Anthony, P F C Vasconcelos, Cristovam Wanderley Picanço Diniz

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
0.2field-weighted citation impact, top 45% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.

  1. Pooled it
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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

7 authors at 5 institutions in 2 countries.

J Bento-TorresLaboratório de Investigações em Neurodegeneração e Infecção, Hospital Universitário, João de Barros Barreto, Instituto de Ciências Biológicas, Universidade Federal do Pará, Belém, PA, Brazil.
L L SobralUniversidade do Estado do Pará, Centro de Ciências da Saúde, Belém, PA, Brazil.
R R ReisVertebrate Embryology Laboratory, Biomedical Sciences Institute, Health Sciences Center, Federal University of Rio de Janeiro, Rio de Janeiro, RJ, Brazil.ORCID 0000-0001-5877-8710
R B de OliveiraLaboratório de Investigações em Neurodegeneração e Infecção, Hospital Universitário, João de Barros Barreto, Instituto de Ciências Biológicas, Universidade Federal do Pará, Belém, PA, Brazil.
D C AnthonyLab of Experimental Neuropathology, Department of Pharmacology, University of Oxford, Oxford, UK.
P F C VasconcelosDepartamento de Arbovirologia e Febres Hemorrágicas, Instituto Evandro Chagas, Ananindeua, PA, Brazil.
Cristovam Wanderley Picanço DinizLaboratório de Investigações em Neurodegeneração e Infecção, Hospital Universitário, João de Barros Barreto, Instituto de Ciências Biológicas, Universidade Federal do Pará, Belém, PA, Brazil.ORCID 0000-0001-6611-6880
Universidade Federal do Pará · BRInstituto Evandro Chagas · BRUniversidade do Estado do Pará · BRUniversidade Federal do Rio de Janeiro · BRUniversity of Oxford · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Because enriched environment (EE) and exercise increase and aging decreases immune response, we hypothesized that environmental enrichment and aging will, respectively, delay and increase prion disease progression. Mice dorsal striatum received bilateral stereotaxic intracerebral injections of normal or ME7 prion infected mouse brain homogenates. After behavior analysis, animals were euthanized and their brains processed for astrocyte GFAP immunolabeling. Our analysis related to the environmental influence are limited to young adult mice, whereas age influence refers to aged mice raised on standard cages. Burrowing activity began to reduce in ME7-SE two weeks before ME7-EE, while no changes were apparent in ME7 aged mice (ME7-A). Object placement recognition was impaired in ME7-SE, NBH-A, and ME7-A but normal in all other groups. Object identity recognition was impaired in ME7-A. Cluster analysis revealed two morphological families of astrocytes in NBH-SE animals, three in NBH-A and ME7-A, and four in NBH-EE, ME7-SE, and ME7-EE. As compared with control groups, astrocytes from DG and CA3 prion-diseased animals show significant numerical and morphological differences and environmental enrichment did not reverse these changes but induced different morphological changes in GFAP+ hippocampal astroglia. We suggest that environmental enrichment and aging delayed hippocampal-dependent behavioral and neuropathological signs of disease progression.

Indexed as

Behavior, AnimalEnvironmentAgingAnimalsAstrocytesBrainDisease Models, AnimalDisease ProgressionHippocampusImmunoenzyme TechniquesMaleMicePrion Diseases

Identifiers

PMID28243355
PMCPMC5294381
OpenAlexW2582363127

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.