Evidence map›Paper›PMID 33283771›Full record

ArticleIndian journal of pharmacology

Human adipose-derived stem cells reduce receptor-interacting protein 1, receptor-interacting protein 3, and mixed lineage kinase domain-like pseudokinase as necroptotic markers in rat model of Alzheimer's disease.

Mina Eftekharzadeh, Sara Simorgh, Maryam Doshmanziari, Leila Hassanzadeh, Marjan Shariatpanahi

Abstract read
In one paragraph

Article in Indian journal of pharmacology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

8 citing papers in PubMed, 1 synthesis or guideline 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

5 authors.

Mina EftekharzadehDepartment of Anatomy, School of Medicine; Neuroscience Research Center, Iran University of Medical Sciences, Tehran, Iran.
Sara SimorghDepartment of Tissue Engineering and Regenerative Medicine, Faculty of Advanced Technologies in Medicine, Iran University of Medical Sciences, Tehran, Iran.
Maryam DoshmanziariDepartment of Anatomy, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Leila HassanzadehDepartment of Nuclear Medicine, School of Medicine, Rajaie Cardiovascular, Medical and Research Center; Department of Medicinal Chemistry, School of Pharmacy.International Campus, Iran University of Medical Sciences, Tehran, Iran.
Marjan ShariatpanahiDepartment of Toxicology and Pharmacology, School of Pharmacy, International Campus; Neuroscience Research Center, Iran University of Medical Sciences, Tehran, Iran.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesAlzheimer's disease (AD) is a constant, developing brain impairment that is described as the aggregation of misfolded amyloid-beta-peptide (Ab) and abnormal tau protein in the brain. Stem cell therapy became a favorable candidate for the regeneration of neurodegenerative disorders like AD, but there is still shortage of knowledge about the underlying mechanisms. The goal of this survey was the determination of the necroptotic pathway as the possible mechanism for the effect of human adipose-derived stem cells (hADSCs) in the rat model of AD. MATERIALS AND

methodsTwelve rats were consumed, dividing into four groups: Control, sham, AD model and AD + stem cell groups. We utilized Nissl and Thioflavin S staining for determining histological changes and immunofluorescent techniques for evaluating necroptotic markers in different regions of the hippocampus.

resultsThe confirmation of AD model was approved with histological examination. The findings indicated more distinct Thio-S stain and an increased number of dead cells in AD rats comparing to other groups. Alternatively, the dead cells number in the CA3 area significantly lessened in AD + stem cell group comparing to AD group. Data showed that hADSCs significantly decreased the expression of necroptotic markers (receptor-interacting protein 1, receptor-interacting protein 3 and mixed lineage kinase domain-like pseudokinase (MLKL)) in AD + stem cell group compared to AD group in different regions of the hippocampus.

conclusionOur findings revealed that the intravenous injection of hADSCs reduced necroptosis and consequently declined the death of neuronal cells in the hippocampus of AD rats.

Indexed as

NecroptosisAlzheimer DiseaseAnimalsBiomarkersDisease Models, AnimalHippocampusHumansMaleMesenchymal Stem Cell TransplantationNeuronsProtein KinasesProtein Serine-Threonine KinasesRatsRats, WistarReceptor-Interacting Protein Serine-Threonine KinasesBiomarkersMLKL protein, ratProtein KinasesProtein Serine-Threonine KinasesReceptor-Interacting Protein Serine-Threonine KinasesRIPK1 protein, ratRipk3 protein, ratAlzheimer diseasemesenchymal stem cell transplantationmixed lineage kinase domain-like pseudo kinase proteinreceptor-interacting protein 1 proteinreceptor-interacting protein 3

Identifiers

PMID33283771
PMCPMC8025767

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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.