Evidence map›Paper›PMID 30673958›Full record

ArticleNeurochemical research2019

The Administration of Cadmium for 2, 3 and 4 Months Causes a Loss of Recognition Memory, Promotes Neuronal Hypotrophy and Apoptosis in the Hippocampus of Rats.

Guadalupe Pulido, Samuel Treviño, Eduardo Brambila, Ruben Vazquez-Roque, Albino Moreno-Rodriguez, Ulises Peña Rosas, Jose Luis Moran-Perales, Anhabella Handal Silva, Jorge Guevara, Gonzalo Flores and 1 more

Abstract read
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In one paragraph

Article in Neurochemical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.6field-weighted citation impact, top 12% 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

12 citing papers in PubMed, 38 citations in OpenAlex.

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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 2 institutions in 1 country.

Guadalupe PulidoFacultad de Ciencias Químicas, Benemérita Universidad Autónoma de Puebla, Puebla, Pue., Mexico.
Samuel TreviñoFacultad de Ciencias Químicas, Benemérita Universidad Autónoma de Puebla, Puebla, Pue., Mexico.
Eduardo BrambilaFacultad de Ciencias Químicas, Benemérita Universidad Autónoma de Puebla, Puebla, Pue., Mexico.
Ruben Vazquez-RoqueLaboratorio de Neuropsiquiatría, Instituto de Fisiología, Benemérita Universidad Autónoma de Puebla, Puebla, Pue., Mexico.
Albino Moreno-RodriguezFacultad de Ciencias Químicas, Benemérita Universidad Autónoma de Puebla, Puebla, Pue., Mexico.
Ulises Peña RosasFacultad de Ciencias Químicas, Benemérita Universidad Autónoma de Puebla, Puebla, Pue., Mexico.
Jose Luis Moran-PeralesLaboratorio de Biología y Toxicología de la Reproducción, Instituto de Ciencias, Benemérita Universidad Autónoma de Puebla, Puebla, Pue., Mexico.
Anhabella Handal SilvaLaboratorio de Biología y Toxicología de la Reproducción, Instituto de Ciencias, Benemérita Universidad Autónoma de Puebla, Puebla, Pue., Mexico.
Jorge GuevaraDepartamento de Bioquímica, Facultad de Medicina, Universidad Nacional Autónoma de México, Mexico City, Mexico.
Gonzalo FloresLaboratorio de Biología y Toxicología de la Reproducción, Instituto de Ciencias, Benemérita Universidad Autónoma de Puebla, Puebla, Pue., Mexico.
Alfonso DiazFacultad de Ciencias Químicas, Benemérita Universidad Autónoma de Puebla, Puebla, Pue., Mexico. alfonso.diaz@correo.buap.mx.ORCID http://orcid.org/0000-0003-4092-6636
Benemérita Universidad Autónoma de Puebla · MXUniversidad Nacional Autónoma de México · MX

Funding

PAPIIT-UNAM IN214117VIEP-BUAP grant No. DIFA-NAT17-IVIEP-BUAP grant TEMS-NAT17-I
6 · The paper itself

Abstract

Cadmium (Cd) is a toxic metal and classified as a carcinogen whose exposure could affect the function of the central nervous system. There are studies that suggest that Cd promotes neurodegeneration in different regions of the brain, particularly in the hippocampus. It is proposed that its mechanism of toxicity maybe by an oxidative stress pathway, which modifies neuronal morphology and causes the death of neurons and consequently affecting cognitive tasks. However, this mechanism is not yet clear. The aim of the present work was to study the effect of Cd administration on recognition memory for 2, 3 and 4 months, neuronal morphology and immunoreactivity for caspase-3 and 9 in rat hippocampi. The results show that the administration of Cd decreased recognition memory. Likewise, it caused the dendritic morphology of the CA1, CA3 and dentate gyrus regions of the hippocampus to decrease with respect to the time of administration of this heavy metal. In addition, we observed a reduction in the density of dendritic spines as well as an increase in the immunoreactivity of caspase-3 and 9 in the same hippocampal regions of the animals treated with Cd. These results suggest that Cd affects the structure and function of the neurons of the hippocampus, which contribute to the deterioration of recognition memory. Our results suggest that the exposure to Cd represents a critical health problem, which if not addressed quickly, could cause much more serious problems in the quality of life of the human population, as well as in the environment in which they develop.

Indexed as

AnimalsApoptosisCadmiumDendritesDendritic SpinesDentate GyrusHippocampusMaleMemoryNeuronsRats, WistarCadmiumCA1–CA3–DG hippocampusCaspasesCell deathDendritic spinesGolgi–CoxThe novel object recognition

Identifiers

PMID30673958
OpenAlexW2911561292

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.