Evidence map›Paper›PMID 36422510›Full record

ArticleTurkish journal of medical sciences2022

Determination of miR-373 and miR-204 levels in neuronal exosomes in Alzheimer's disease.

Elifcan Taşdelen, Erguvan Tuğba Özel Kızıl, Sabiha Tezcan, Eray Yalap, Ayşe Petek Bingöl, Nüket Yürür Kutlay

Open access · bronzeAbstract read
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Article in Turkish journal of medical sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 2 pooled it
1.9field-weighted citation impact, top 13% 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

15 citing papers in PubMed, 2 syntheses or guidelines pooled it, 24 citations in OpenAlex.

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  5. Extracellular Vesicles in Tauopathies: Mechanisms and Applications.International journal of molecular sciences · 2026
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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

6 authors at 2 institutions in 2 countries.

Elifcan TaşdelenDepartment of Medical Genetics, Faculty of Medicine, Ankara University, Ankara, Turkey ; Department of Medical Genetics, Şanlıurfa Training and Research Hospital, Şanlıurfa, Turkey.
Erguvan Tuğba Özel KızılDepartment of Psychiatry, Faculty of Medicine, Ankara University, Ankara, Turkey.
Sabiha TezcanDepartment of Neurology, Faculty of Medicine, Ankara University, Ankara, Turkey ; Department of Neurology, Dr. Nafiz Körez Sincan State Hospital, Ankara, Turkey.
Eray YalapDepartment of Neurology, Faculty of Medicine, Ankara University, Ankara, Turkey.
Ayşe Petek BingölDepartment of Neurology, Faculty of Medicine, Ankara University, Ankara, Turkey.
Nüket Yürür KutlayDepartment of Medical Genetics, Faculty of Medicine, Ankara University, Ankara, Turkey.
Ankara University · TRMedical Genetics Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNLRP3 inflammasome activation has been known to be involved in the etiology and progression of Alzheimer's disease (AD). Furthermore, AD and diabetes mellitus have common pathomechanisms. It has been shown that P2X7R whose expression is increased in brain tissues with AD and plays a role in the activation of NLRP3 inflammasome is suppressed by miR-373 in patients with osteoarthritis. Therefore, the question of whether the suppressive effect of miR-373 on NLRP3 may have a role in the pathophysiology of AD comes to mind. On the other hand, it is known that the miR-204 level increases in response to TXNIP, another NLRP3 inflammasome inducer with high expression in AD. In primary human islets, miR-204 reduces the expression of GLP-1R. It has been discovered that in vivo deletion of miR-204 is protective against diabetes by increasing GLP-1R and insulin secretion. Considering the relationship between miR-204 and TXNIP and the relationship of miR-204 with diabetes suggests investigating the effect of miR-204 on the inflammatory pathway in AD. Based on the common pathophysiological mechanisms between AD and diabetes and the reported changes related to NLRP3 inflammasome, we analyzed miR-373 and miR-204 in neuron-derived serum exosomes in this study. Neuron-derived exosomes in neurodegenerative diseases are considered to be better candidates for developing potential biomarkers.

methodsThe expression levels of miR-204 and miR-373 were investigated in neuron-derived serum exosomes obtained from 15 patients with mild AD, 18 with moderate AD, and 21 cognitively healthy individuals.

resultsThe miR-204 and miR-373 expressions were significantly decreased in both patient groups compared to the control group. Therefore, we suggest that miR-204 and miR-373 are potential biomarkers for AD. However, due to the preliminary nature of this study, further large-scale studies are needed to support our findings.

Indexed as

Alzheimer DiseaseExosomesMicroRNAsBiomarkersHumansInflammasomesNeuronsNLR Family, Pyrin Domain-Containing 3 ProteinBiomarkersInflammasomesMicroRNAsMIRN204 microRNA, humanMIRN373 microRNA, humanNLR Family, Pyrin Domain-Containing 3 ProteinAlzheimer’s diseaseGLP-1RMiR-204miR-373neuron derived exosomesNLRP3 inflammasomeP2X7RTXNIP

Identifiers

PMID36422510
PMCPMC10395704
OpenAlexW4310334685

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.