Evidence map›Paper›PMID 31853828›Full record

ArticleMetabolic brain disease2020

Effects of vitamin D in an animal model of Alzheimer's disease: behavioral assessment with biochemical investigation of Hippocampus and serum.

Negar Mehri, Rasool Haddadi, Maziar Ganji, Siamak Shahidi, Sara Soleimani Asl, Masoume Taheri Azandariani, Akram Ranjbar

Abstract read
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In one paragraph

Article in Metabolic brain disease, 2020. 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
1.2field-weighted citation impact, top 24% 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, 32 citations in OpenAlex.

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  11. Genome-Protecting Compounds as Potential Geroprotectors.International journal of molecular sciences · 2020
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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 2 institutions in 1 country.

Negar MehriDepartment of Toxicology and Pharmacology, School of Pharmacy, Hamadan University of Medical Sciences, Hamadan, Iran.
Rasool HaddadiDepartment of Toxicology and Pharmacology, School of Pharmacy, Hamadan University of Medical Sciences, Hamadan, Iran.
Maziar GanjiDepartment of Medical Genetics, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Siamak ShahidiNeurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran.
Sara Soleimani AslDepartment of Anatomy, School of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran.
Masoume Taheri AzandarianiNeurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran.
Akram RanjbarDepartment of Toxicology and Pharmacology, School of Pharmacy, Hamadan University of Medical Sciences, Hamadan, Iran. akranjbar2015@gmail.com.
Hamedan University of Medical Sciences · IRShahid Beheshti University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Regulatory role of vitamin D (VitD) in cognitive memory and learning has been proposed. Here, we examine the behavioral and biochemical effects of VitD in Alzheimer's disease (AD), as the most common form of dementia, in male Wistar rats. Animals (n = 48) were randomly divided into six groups: control, sham solvent, sham surgery, VitD (by intraperitoneal injection), AD (receiving intrahippocampal injection of amyloid-beta peptide, Aβ), and combination of VitD and Aβ. Learning and memory functions were investigated through the passive avoidance and the Morris water maze (MWM) tasks. Moreover, oxidative stress biomarkers including total antioxidant capacity (TAC), total thiol groups (TTG), lipid peroxidation (LPO), and DNA damage were assessed in hippocampus and serum. In passive avoidance task, Aβ significantly impaired the step-through latency and time in dark compartment. It also increased escape latency and time spent in the target quadrant in the MWM. VitD administration attenuated the Aβ-induced memory impairment in passive avoidance and MWM tests. Furthermore, VitD reduced deleterious biochemical effect of Aβ by enhancing the levels of TAC and TTG in addition to decreasing LPO and DNA damage levels in both hippocampus and serum. We showed, for the first time, that VitD administration improves the impaired Aβ-induced memory and that, by acting as a strong antioxidant, it can attenuate the stress oxidative biomarkers in hippocampus and serum of rats with AD. Altogether, our results provide evidence for further application of VitD in neurodegenerative disorders such as AD to enlighten the involved mechanisms.

Indexed as

Disease Models, AnimalAlzheimer DiseaseAmyloid beta-PeptidesAnimalsAvoidance LearningHippocampusLipid PeroxidationMaleRandom AllocationRatsRats, WistarTreatment OutcomeVitamin DAmyloid beta-PeptidesVitamin DAlzheimer’s diseaseAmyloid-betaHippocampusOxidative stressVitamin D

Identifiers

PMID31853828
OpenAlexW2996061623

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.