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miR-361-5p contributes to the pathogenesis of Alzheimer's disease.

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Název: miR-361-5p contributes to the pathogenesis of Alzheimer's disease.
Autoři: Jalaiei A; Department of Medical Genetics, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran., Gharesouran J; Department of Medical Genetics, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran., Arsang-Jang S; Cancer Gene Therapy Research Center, Zanjan University of Medical Sciences, Zanjan, Iran., Talebi M; Neurosciences Research Center (NSRC), Tabriz University of Medical Sciences, Tabriz, Iran., Rezazadeh M; Department of Medical Genetics, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran. Rezazadeh.mary@gmail.com., Ghafouri-Fard S; Department of Medical Genetics, Shahid Beheshti University of Medical Sciences, Tehran, Iran. s.ghafourifard@sbmu.ac.ir.
Zdroj: Scientific reports [Sci Rep] 2025 Aug 23; Vol. 15 (1), pp. 31046. Date of Electronic Publication: 2025 Aug 23.
Způsob vydávání: Journal Article
Jazyk: English
Informace o časopise: Publisher: Nature Publishing Group Country of Publication: England NLM ID: 101563288 Publication Model: Electronic Cited Medium: Internet ISSN: 2045-2322 (Electronic) Linking ISSN: 20452322 NLM ISO Abbreviation: Sci Rep Subsets: MEDLINE
Imprint Name(s): Original Publication: London : Nature Publishing Group, copyright 2011-
Výrazy ze slovníku MeSH: Alzheimer Disease*/genetics , Alzheimer Disease*/pathology , Alzheimer Disease*/metabolism , MicroRNAs*/genetics , MicroRNAs*/metabolism, Humans ; Male ; Female ; Aged ; Homer Scaffolding Proteins/genetics ; Homer Scaffolding Proteins/metabolism ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Middle Aged ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Biomarkers ; Brain/metabolism ; Brain/pathology ; Gene Expression Regulation ; Aged, 80 and over
Abstrakt: Competing Interests: Declaration. Competing interests: The authors declare no competing interests. Ethics approval and consent to participate: Human participants in the study received approval from the Tabriz University of Medical Sciences Clinical Research Ethics Committee (Ethical code: IR.TBZMED.REC.1398.1265). All patients/participants provided written informed consent to participate in the study. All methods were performed by relevant guidelines and regulations. Informed consent: Informed consent has been obtained from all patients.
Alzheimer's disease (AD) is a progressive neurodegenerative disorder. This study investigated the roles of HOMER1, ATAD1, and miR-361 in AD pathogenesis using microarray (GSE106241, GSE157239; n = 60) and RT-PCR (n = 100; 50 AD patients, 50 controls from Northwest Iran) analyses. Decreased expression of HOMER1 and ATAD1, key regulators of glutamatergic synapses, and miR-361, a potential regulator of both, was observed in AD brain tissue (GSE106241, categorized into seven Braak stages), suggesting a link between their dysregulation, impaired synaptic function, and increased neuroinflammation. However, blood-based RT-PCR showed no significant difference in HOMER1 or ATAD1. miR-361 was significantly lower in AD patients (adjusted p < 0.043). These findings, limited by sample size and lacking a formal power analysis, require further investigation to validate their potential as peripheral biomarkers for AD. Future studies with larger sample sizes are warranted.
(© 2025. The Author(s).)
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Contributed Indexing: Keywords: ATAD1; HOMER1; MIR-361; Alzheimer’s disease; Glutamatergic synapses
Substance Nomenclature: 0 (MicroRNAs)
0 (MIRN361 microRNA, human)
0 (Homer Scaffolding Proteins)
0 (HOMER1 protein, human)
0 (DNA-Binding Proteins)
0 (Membrane Proteins)
0 (Biomarkers)
Entry Date(s): Date Created: 20250823 Date Completed: 20250823 Latest Revision: 20250827
Update Code: 20250903
PubMed Central ID: PMC12374966
DOI: 10.1038/s41598-025-17112-z
PMID: 40849350
Databáze: MEDLINE
Popis
Abstrakt:Competing Interests: Declaration. Competing interests: The authors declare no competing interests. Ethics approval and consent to participate: Human participants in the study received approval from the Tabriz University of Medical Sciences Clinical Research Ethics Committee (Ethical code: IR.TBZMED.REC.1398.1265). All patients/participants provided written informed consent to participate in the study. All methods were performed by relevant guidelines and regulations. Informed consent: Informed consent has been obtained from all patients.<br />Alzheimer's disease (AD) is a progressive neurodegenerative disorder. This study investigated the roles of HOMER1, ATAD1, and miR-361 in AD pathogenesis using microarray (GSE106241, GSE157239; n = 60) and RT-PCR (n = 100; 50 AD patients, 50 controls from Northwest Iran) analyses. Decreased expression of HOMER1 and ATAD1, key regulators of glutamatergic synapses, and miR-361, a potential regulator of both, was observed in AD brain tissue (GSE106241, categorized into seven Braak stages), suggesting a link between their dysregulation, impaired synaptic function, and increased neuroinflammation. However, blood-based RT-PCR showed no significant difference in HOMER1 or ATAD1. miR-361 was significantly lower in AD patients (adjusted p &lt; 0.043). These findings, limited by sample size and lacking a formal power analysis, require further investigation to validate their potential as peripheral biomarkers for AD. Future studies with larger sample sizes are warranted.<br /> (© 2025. The Author(s).)
ISSN:2045-2322
DOI:10.1038/s41598-025-17112-z