Evidence map›Paper›PMID 37665469›Full record

ArticleMetabolic brain disease2023

Expression analysis of inhibitory B7 family members in Alzheimer's disease.

Hani Sabaie, Parham Tamimi, Jalal Gharesouran, Zoha Salkhordeh, Mohammad Reza Asadi, Mirmohsen Sharifi-Bonab, Zeinab Shirvani-Farsani, Mohammad Taheri, Arezou Sayad, Maryam Rezazadeh

Abstract read
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Article in Metabolic brain disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 39% 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

3 citing papers in PubMed, 2 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

10 authors at 5 institutions in 2 countries.

Hani Sabaie *Clinical Research Development Unit of Tabriz Valiasr Hospital, Tabriz University of Medical Sciences, Tabriz, Iran.ORCID 0000-0001-7678-8357
Parham Tamimi *School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID 0000-0002-0294-8722
Jalal GharesouranDepartment of Medical Genetics, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.ORCID 0000-0002-2613-3421
Zoha SalkhordehDepartment of Medical Genetics, Faculty of Medicine, Kerman University of Medical Sciences, Kerman, Iran.ORCID 0009-0008-0152-0661
Mohammad Reza AsadiClinical Research Development Unit of Tabriz Valiasr Hospital, Tabriz University of Medical Sciences, Tabriz, Iran.ORCID 0000-0002-7055-9550
Mirmohsen Sharifi-BonabClinical Research Development Unit of Tabriz Valiasr Hospital, Tabriz University of Medical Sciences, Tabriz, Iran.
Zeinab Shirvani-FarsaniDepartment of Cell and Molecular Biology, Faculty of Life Sciences and Technology, Shahid Beheshti University, Tehran, Iran.ORCID 0000-0003-2071-1208
Mohammad TaheriInstitute of Human Genetics, Jena University Hospital, Jena, Germany. rezazadehm@tbzmed.ac.ir.ORCID 0000-0001-8381-0591
Arezou SayadDepartment of Medical Genetics, Loghman Hakim Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran. ar.sayad@yahoo.com.ORCID 0000-0002-9417-6466
Maryam RezazadehClinical Research Development Unit of Tabriz Valiasr Hospital, Tabriz University of Medical Sciences, Tabriz, Iran. mohammad_823@yahoo.com.ORCID 0000-0002-0790-1317
Tabriz University of Medical Sciences · IRShahid Beheshti University of Medical Sciences · IRJena University Hospital · DEKerman University of Medical Sciences · IRShahid Beheshti University · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a global health problem due to its complexity, which frequently makes the development of treatment methods extremely difficult. Therefore, new methodologies are necessary to investigate the pathophysiology of AD and to treat AD. The interaction of immune modulation and neurodegeneration has added new dimensions in current knowledge of AD etiology and offers an attractive opportunity for the discovery of novel biomarkers and therapies. Using quantitative polymerase chain reaction, we compared the expression levels of inhibitory B7 family members (B7-1, B7-2, B7-H1, B7-DC, B7-H3, B7-H4, B7-H5, B7-H7, and ILDR2), as immune regulators, in the peripheral blood of late-onset AD (LOAD) patients (n = 50) and healthy individuals (n = 50). The levels of B7-2, B7-H4, ILDR2, and B7-DC expression were significantly higher in-patient blood samples than in control blood samples. Furthermore, we discovered a substantial positive correlation between all gene expression levels. In addition, the current study indicated that ILDR2, B7-H4, B7-2, and B7-DC might serve as diagnostic biomarkers to identify LOAD patients from healthy persons. The present work provides additional evidence for the significance of inhibitory B7 family members to the etiology of LOAD.

Indexed as

Alzheimer DiseaseV-Set Domain-Containing T-Cell Activation Inhibitor 1BiomarkersHumansBiomarkersV-Set Domain-Containing T-Cell Activation Inhibitor 1Alzheimer’s diseaseB7 familyBiomarkerExpression analysisImmune checkpoint

Identifiers

PMID37665469
OpenAlexW4386407638

What OpenQuestion holds

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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.