Evidence map›Paper›PMID 24586614›Full record

ArticlePloS one2014

Central proliferation and neurogenesis is impaired in type 2 diabetes and prediabetes animal models.

Juan Jose Ramos-Rodriguez, Sara Molina-Gil, Oscar Ortiz-Barajas, Margarita Jimenez-Palomares, German Perdomo, Irene Cozar-Castellano, Alfonso Maria Lechuga-Sancho, Monica Garcia-Alloza

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
6.9field-weighted citation impact, top 2% 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

55 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.

  1. Pooled it
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  20. Frontiers in pharmacology · 2022
    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

8 authors at 4 institutions in 1 country.

Juan Jose Ramos-RodriguezDivision of Physiology, Dpt. Biomedicine, Biotechnology and Public Health, Institute of Biomolecules (INBIO), School of Medicine, University of Cadiz, Cadiz, Spain.
Sara Molina-GilDivision of Physiology, Dpt. Biomedicine, Biotechnology and Public Health, Institute of Biomolecules (INBIO), School of Medicine, University of Cadiz, Cadiz, Spain.
Oscar Ortiz-BarajasDivision of Physiology, Dpt. Biomedicine, Biotechnology and Public Health, Institute of Biomolecules (INBIO), School of Medicine, University of Cadiz, Cadiz, Spain.
Margarita Jimenez-PalomaresInstitute de Biology and Molecular Genetics, University of Valladolid-CSIC, Valladolid, Spain.
German PerdomoDpt. of Inorganic and Organic Chemistry, and Biochemistry, University of Castilla La Mancha, Toledo, Spain.
Irene Cozar-CastellanoInstitute de Biology and Molecular Genetics, University of Valladolid-CSIC, Valladolid, Spain.
Alfonso Maria Lechuga-SanchoDepartment of Pediatrics, School of Medicine, University of Cadiz, Cadiz, Spain.
Monica Garcia-AllozaDivision of Physiology, Dpt. Biomedicine, Biotechnology and Public Health, Institute of Biomolecules (INBIO), School of Medicine, University of Cadiz, Cadiz, Spain.
Universidad de Cádiz · ESInstituto de Biomedicina y Genética Molecular de Valladolid · ESUniversidad de Valladolid · ESUniversity of Castilla-La Mancha · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 2 diabetes (T2D) is an important risk factor to suffer dementia, including Alzheimer's disease (AD), and some neuropathological features observed in dementia could be mediated by T2D metabolic alterations. Since brain atrophy and impaired neurogenesis have been observed both T2D and AD we analyzed central nervous system (CNS) morphological alterations in the db/db mice (leptin receptor KO mice), as a model of long-term insulin resistance and T2D, and in C57Bl6 mice fed with high fat diet (HFD), as a model of diet induced insulin resistance and prediabetes. Db/db mice showed an age-dependent cortical and hippocampal atrophy, whereas in HFD mice cortex and hippocampus were preserved. We also detected increased neurogenesis and cell proliferation rates in young db/db mice when compared with control littermates. Our study shows that metabolic parameters serve as predictors of both atrophy and altered proliferation and neurogenesis in the CNS. Moreover in the cortex, atrophy, cell proliferation and neurogenesis were significantly correlated. Our data suggest that T2D may underline some of the pathological features observed in the dementia process. They also support that blood glucose control in elderly patients could help to slow down dementia evolution and maybe, improve its prognosis.

Indexed as

Cell ProliferationDisease Models, AnimalAnimalsBlood GlucoseBrainDiabetes Mellitus, Type 2Diet, High-FatImmunoenzyme TechniquesInsulinInsulin ResistanceMaleMiceMice, KnockoutMice, ObeseNeurogenesisPrediabetic StateBlood GlucoseInsulinleptin receptor, mouseReceptors, Leptin

Identifiers

PMID24586614
PMCPMC3930705
OpenAlexW2058606198

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.