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Alzheimer's disease (AD) is a neurodegenerative disorder that progresses over time and is identified by the development of neurofibrillary tangles and amyloid deposits in the brain. Mounting evidence has revealed that microRNAs (miRNAs) are significantly involved in AD progression, and may be used as promising biomarkers for diagnosis and prognosis. Nevertheless, the existing body of data regarding dysregulated circulating miRNAs in AD and their therapeutic applications are characterized by a lack of consistency. A comprehensive search was performed across various databases (PubMed, EMBASE, Web of Science, Scopus, Google Scholar, Cochrane, and ProQuest), starting from its inception and ending in January 2023. The criteria for inclusion consisted of original research studies written in English, which utilized Real-Time PCR to analyze miRNA expression in the blood, serum, or plasma of AD patients and healthy controls. The extracted data included the miRNA(s) investigated, dysregulation status, study type, human sample(s), and major findings. The search produced 608 records, which after careful examination, resulted in 48 suitable articles for data extraction. The research revealed a wide range of sample types used, with whole blood (39.59%) and serum (27.09%, including serum-exosome at 4.17%) emerging as the most prominent. The compiled dataset featured 4001 AD patients and 3886 healthy controls, revealing intricate regulatory patterns among 83 up-regulated (35.78%), 66 down-regulated (28.44%), and 83 not significantly altered (35.78%) miRNAs. Our results demonstrated that specific circulating miRNAs are consistently dysregulated in AD and could serve as non-intrusive biomarkers for the identification, prognosis, and prediction of cognitive decline. Further large-scale prospective studies are required to validate their clinical applications., Competing Interests: Declarations. Competing interests: The authors declare no competing interests. Ethical approval: Kindly note that this study is a systematic review, which, by its nature, does not involve direct interaction with human subjects, animals, or the collection of primary data. Therefore, ethical approval was not pursued for this review. The research methodology adheres to ethical considerations, as it focuses on a comprehensive synthesis and analysis of previously published and publicly available information. This approach ensures alignment with ethical standards and guidelines, while providing valuable insights into the existing body of knowledge on the subject. Your understanding and consideration regarding this matter are sincerely appreciated. Consent to participate: Not applicable. Consent for publication: Not applicable., (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Schizophrenia (SCZ) is a severe mental disorder with an unknown pathophysiology. Brain-Derived Neurotrophic Factor (BDNF) is a neurotrophin that has been associated with synapse plasticity, learning, and memory, as well as neurodevelopment and neuroprotection. The importance of neurodevelopmental and neurotoxicity-related components in the pathophysiology of SCZ has been highlighted in research on the neurobiology of this disease. The purpose of this research is to investigate the significant expression of two variables, tristetraprolin (TTP) and miR-16, which are known to be regulators of BDNF expression. Fifty Iranian Azeri SCZ patients were enrolled, and fifty healthy volunteers were age- and gender-matched as controls. A quantitative polymerase chain reaction measured the expression levels of the TTP and miR-16 in the peripheral blood (PB) of SCZ patients and healthy people. TTP expression levels in patients were higher than in controls, regardless of gender or age (posterior beta = 1.532, adjusted P-value = 0.012). TTP and miR-16 expression levels were found to be significantly correlated in both SCZ patients and healthy controls (r = 0.701, P < 0.001 and r = 0.777, P < 0.001, respectively). Due to the increased expression of TTP in SCZ and the existence of a significant correlation between TTP and miR-16, which helps to act on target mRNAs with AU-rich elements, this mechanism can be considered an influencing factor in SCZ., (© 2022. The Author(s).)

Schizophrenia (SCZ) is known as a complicated mental disease with an unknown etiology. The microdeletion of 22q11.2 is the most potent genetic risk factor. Researchers are still trying to find which genes in the deletion region are linked to SCZ. MIR185, encoding microRNA (miR)-185, is present in the minimal 1.5 megabase deletion. Nonetheless, the miR-185 expression profile and its corresponding target genes in animal models and patients with 22q11.2 deletion syndrome (22q11.2DS) imply that more study is required about miR-185 and its corresponding downstream pathways within idiopathic SCZ. The expression of hsa-miR-185-5p and its corresponding target gene, shisa family member 7 (SHISA7), sometimes called CKAMP59, were evaluated in the peripheral blood (PB) samples of Iranian Azeri patients with idiopathic SCZ and healthy subjects, matched by gender and age as control groups by quantitative polymerase chain reaction (qPCR). Fifty SCZ patients (male/female: 22/28, age (mean ± standard deviation (SD)): 35.9 ± 5.6) and 50 matched healthy controls (male/female: 23/27, age (mean ± SD): 34.7 ± 5.4) were enrolled. The expression of hsa-miR-185-5p in the PB samples from subjects with idiopathic SCZ was substantially lower than in that of control groups (posterior beta = -0.985, adjusted P-value < 0.0001). There was also a difference within the expression profile between female and male subgroups (posterior beta = -0.86, adjusted P-value = 0.046 and posterior beta = -1.015, adjusted P-value = 0.004, in turn). Nevertheless, no significant difference was present in the expression level of CKAMP59 between PB samples from patients and control groups (adjusted P-value > 0.999). The analysis of the receiver operating characteristic (ROC) curve suggested that hsa-miR-185-5p may correctly distinguish subjects with idiopathic SCZ from healthy people (the area under curve (AUC) value: 0.722). Furthermore, there was a strong positive correlation between the expression pattern of the abovementioned genes in patients with SCZ and healthy subjects (r = 0.870, P < 0.001 and r = 0.812, P < 0.001, respectively), indicating that this miR works as an enhancer. More research is needed to determine if the hsa-miR-185-5p has an enhancer activity. In summary, this is the first research to highlight the expression of the miR-185 and CKAMP59 genes in the PB from subjects with idiopathic SCZ. Our findings suggest that gene expression alterations mediated by miR-185 may play a role in the pathogenesis of idiopathic and 22q11.2DS SCZ. It is worth noting that, despite a substantial and clear relationship between CKAMP59 and hsa-miR-185-5p, indicating an interactive network, their involvement in the development of SCZ should be reconsidered based on the whole blood sample since the changed expression level of CKAMP59 was not significant. Further research with greater sample sizes and particular leukocyte subsets can greatly make these results stronger., (© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

The etiology of schizophrenia (SCZ), as a serious mental illness, is unknown. The significance of genetics in SCZ pathophysiology is yet unknown, and newly identified mechanisms involved in the regulation of gene transcription may be helpful in determining how these changes affect SCZ development and progression. In the current work, we used a bioinformatics approach to describe the role of long non-coding RNA (lncRNA)-associated competing endogenous RNAs (ceRNAs) in the olfactory epithelium (OE) samples in order to better understand the molecular regulatory processes implicated in SCZ disorders in living individuals. The Gene Expression Omnibus database was used to obtain the OE microarray dataset (GSE73129) from SCZ sufferers and control subjects, which contained information about both lncRNAs and mRNAs. The limma package of R software was used to identify the differentially expressed lncRNAs (DElncRNAs) and mRNAs (DEmRNAs). RNA interaction pairs were discovered using the Human MicroRNA Disease Database, DIANA-LncBase, and miRTarBase databases. In this study, the Pearson correlation coefficient was utilized to find positive correlations between DEmRNAs and DElncRNAs in the ceRNA network. Eventually, lncRNA-associated ceRNA axes were developed based on co-expression relations and DElncRNA-miRNA-DEmRNA interactions. This work found six potential DElncRNA-miRNA-DEmRNA loops in SCZ pathogenesis, including, SNTG2-AS1/hsa-miR-7-5p/SLC7A5, FLG-AS1/hsa-miR-34a-5p/FOSL1, LINC00960/hsa-miR-34a-5p/FOSL1, AQP4-AS1/hsa-miR-335-5p/FMN2, SOX2-OT/hsa-miR-24-3p/NOS3, and CASC2/hsa-miR-24-3p/NOS3. According to the findings, ceRNAs in OE might be promising research targets for studying SCZ molecular mechanisms. This could be a great opportunity to examine different aspects of neurodevelopment that may have been hampered early in SCZ patients., (© 2021. The Author(s).)

Multiple sclerosis (MS) is an immune-mediated demyelinating and degenerative disease with unknown etiology. Inappropriate response of T-cells to myelin antigens has an essential role in the pathophysiology of MS. The clinical and pathophysiological complications of MS necessitate identification of potential molecular targets to understand the pathogenic events of MS. Since the functions and regulatory mechanisms of long non-coding RNAs (lncRNAs) acting as competing endogenous RNAs (ceRNAs) in MS are yet uncertain, we conducted a bioinformatics analysis to explain the lncRNA-associated ceRNA axes to clarify molecular regulatory mechanisms involved in T-cells responses in MS. Two microarray datasets of peripheral blood T-cell from subjects with relapsing-remitting MS and matched controls containing data about miRNAs (GSE43590), mRNAs and lncRNAs (GSE43591) were downloaded from the Gene Expression Omnibus database. Differentially expressed miRNAs (DEmiRNAs), mRNAs (DEmRNAs), and lncRNAs (DElncRNAs) were identified by the limma package of the R software. Protein-protein interaction (PPI) network and module were developed using the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) and the Molecular Complex Detection (MCODE) Cytoscape plugin, respectively. Using DIANA-LncBase and miRTarBase, the lncRNA-associated ceRNA axes was constructed. We conducted a Pearson correlation analysis and selected the positive correlations among the lncRNAs and mRNAs in the ceRNA axes. Lastly, DEmRNAs pathway enrichment was conducted by the Enrichr tool. A ceRNA regulatory relationship among Small nucleolar RNA host gene 1 ( SNHG1 ), hsa-miR-197-3p , YOD1 deubiquitinase ( YOD1 ) and zinc finger protein 101 ( ZNF101 ) and downstream connected genes was identified. Pathway enrichment analysis showed that DEmRNAs were enriched in "Protein processing in endoplasmic reticulum" and "Herpes simplex virus 1 infection" pathways. To our knowledge, this would be the first report of a possible role of SNHG1 / hsa-miR-197-3p / YOD1 / ZNF101 axes in the pathogenesis of MS. This research remarks on the significance of ceRNAs and prepares new perceptions for discovering the molecular mechanism of MS., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Sabaie, Salkhordeh, Asadi, Ghafouri-Fard, Amirinejad, Askarinejad Behzadi, Hussen, Taheri and Rezazadeh.)

Alzheimer’s disease (AD) is a neurodegenerative disorder that progresses over time and is identified by the development of neurofibrillary tangles and amyloid deposits in the brain. Mounting evidence has revealed that microRNAs (miRNAs) are significantly involved in AD progression, and may be used as promising biomarkers for diagnosis and prognosis. Nevertheless, the existing body of data regarding dysregulated circulating miRNAs in AD and their therapeutic applications are characterized by a lack of consistency. A comprehensive search was performed across various databases (PubMed, EMBASE, Web of Science, Scopus, Google Scholar, Cochrane, and ProQuest), starting from its inception and ending in January 2023. The criteria for inclusion consisted of original research studies written in English, which utilized Real-Time PCR to analyze miRNA expression in the blood, serum, or plasma of AD patients and healthy controls. The extracted data included the miRNA(s) investigated, dysregulation status, study type, human sample(s), and major findings. The search produced 608 records, which after careful examination, resulted in 48 suitable articles for data extraction. The research revealed a wide range of sample types used, with whole blood (39.59%) and serum (27.09%, including serum-exosome at 4.17%) emerging as the most prominent. The compiled dataset featured 4001 AD patients and 3886 healthy controls, revealing intricate regulatory patterns among 83 up-regulated (35.78%), 66 down-regulated (28.44%), and 83 not significantly altered (35.78%) miRNAs. Our results demonstrated that specific circulating miRNAs are consistently dysregulated in AD and could serve as non-intrusive biomarkers for the identification, prognosis, and prediction of cognitive decline. Further large-scale prospective studies are required to validate their clinical applications. [ABSTRACT FROM AUTHOR]