Beyond the glutamate N-methyl D-aspartate receptor in major depressive disorder: the mTOR signaling pathway / Majör depresif bozuklukta glutamat N-metil-D-aspartat reseptörlerinin ötesi: mTOR sinyal yolağı

2011 ◽  
pp. 1-6 ◽  
Author(s):  
Beata Karolewicz ◽  
Mesut Cetin ◽  
Feyza Aricioglu
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Signaling Pathway ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Major Depressive ◽  
Aspartate Receptor

scholarly journals The mTOR signaling pathway in the prefrontal cortex is compromised in major depressive disorder

2011 ◽  
Vol 35 (7) ◽  
pp. 1774-1779 ◽  
Author(s):  
Courtney S. Jernigan ◽  
Dharmendra B. Goswami ◽  
Mark C. Austin ◽  
Abiye H. Iyo ◽  
Agata Chandran ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Prefrontal Cortex ◽  
Depressive Disorder ◽  
Signaling Pathway ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Major Depressive

scholarly journals Ketamine for the treatment of major depressive disorder and bipolar depression: A review of the literature

2017 ◽  
Vol 7 (1) ◽  
pp. 16-23 ◽  
Author(s):  
Sarah E. Grady ◽  
Travis A. Marsh ◽  
Allison Tenhouse ◽  
Kelsey Klein
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Bipolar Depression ◽  
Treatment Resistant Depression ◽  
Treatment Resistant ◽  
Major Depressive ◽  
Randomized Controlled ◽  
The Past ◽  
Aspartate Receptor ◽  
Resistant Depression

Abstract Introduction: Over the past decade, ketamine has been studied for major depressive disorder and bipolar depression. Ketamine is believed to exert its antidepressant properties through N-methyl-D-aspartate receptor antagonism. Methods: Study authors completed a literature review of seven randomized controlled trials of ketamine usage in major depressive disorder and bipolar depression. Results: Ketamine demonstrated a statistically significant improvement over placebo or midazolam in major depressive disorder. Ketamine also exhibited a statistically significant improvement over placebo in bipolar depression. Discussion: Ketamine has shown promise in quickly reducing symptoms in patients with treatment resistant depression and bipolar depression. Using ketamine may be helpful for patients that have exhausted other therapeutic options.

Altered mRNA expressions for N-methyl-D-aspartate receptor-related genes in WBC of patients with major depressive disorder

2019 ◽  
Vol 245 ◽  
pp. 1119-1125 ◽  
Author(s):  
Chieh-Hsin Lin ◽  
Min-Wei Huang ◽  
Ching-Hua Lin ◽  
Chiung-Hsien Huang ◽  
Hsien-Yuan Lane
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Major Depressive ◽  
Aspartate Receptor

Identification of Crucial Genes and Diagnostic Value Analysis in Major Depressive Disorder Using Bioinformatics Analysis

2020 ◽  
Vol 23 ◽  
Author(s):  
Yao Gao ◽  
Huiliang Zhao ◽  
Teng Xu ◽  
Junsheng Tian ◽  
Xuemei Qin
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Signaling Pathway ◽  
Enrichment Analysis ◽  
Functional Enrichment ◽  
Differentially Expressed ◽  
Hub Genes ◽  
Major Depressive ◽  
Diagnostic Ability ◽  
Value Analysis

Aim and Objective:: Despite the prevalence and burden of major depressive disorder (MDD), our current understanding of the pathophysiology is still incomplete. Therefore, this paper aims to explore genes and evaluate their diagnostic ability in the pathogenesis of MDD. Methods:: Firstly, the expression profiles of mRNA and microRNA were downloaded from the gene expression database and analyzed by the GEO2R online tool to identify differentially expressed genes (DEGs) and differentially expressed microRNAs (DEMs). Then, the DAVID tool was used for functional enrichment analysis. Secondly, the comprehensive protein- protein interaction (PPI) network was analyzed using Cytoscape, and the network MCODE was applied to explore hub genes. Thirdly, the receiver operating characteristic (ROC) curve of the core gene was drawn to evaluate clinical diagnostic ability. Finally, mirecords was used to predict the target genes of DEMs. Results:: A total of 154 genes were identified as DEGs, and 14 microRNAs were identified as DEMs. Pathway enrichment analysis showed that DEGs were mainly involved in hematopoietic cell lineage, PI3K-Akt signaling pathway, cytokinecytokine receptor interaction, chemokine signaling pathway, and JAK-STAT signaling pathway. Three important modules are identified and selected by the MCODE clustering algorithm. The top 12 hub genes including CXCL16, CXCL1, GNB5, GNB4, OPRL1, SSTR2, IL7R, MYB, CSF1R, GSTM1, GSTM2, and GSTP1 were identified as important genes for subsequent analysis. Among these important hub genes, GSTM2, GNB4, GSTP1 and CXCL1 have good diagnostic ability. Finally, by combining these four genes, the diagnostic ability of MDD can be improved to 0.905, which is of great significance for the clinical diagnosis of MDD. Conclusion:: Our results indicate that GSTM2, GNB4, GSTP1 and CXCL1 have potential diagnostic markers and are of great significance in clinical research and diagnostic application of MDD. This result needs a large sample study to further confirm the pathogenesis of MDD.

scholarly journals Ketamine, but Not the NMDAR Antagonist Lanicemine, Increases Prefrontal Global Connectivity in Depressed Patients

2018 ◽  
Vol 2 ◽  
pp. 247054701879610 ◽  
Author(s):  
Chadi G. Abdallah ◽  
Arpan Dutta ◽  
Christopher L. Averill ◽  
Shane McKie ◽  
Teddy J. Akiki ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Brain Connectivity ◽  
Acute Effects ◽  
Major Depressive ◽  
Aspartate Receptor ◽  
Global Signal ◽  
Global Brain ◽  
The Relationship

Background Identifying the neural correlates of ketamine treatment may facilitate and expedite the development of novel, robust, and safe rapid-acting antidepressants. Prefrontal cortex (PFC) global brain connectivity with global signal regression (GBCr) was recently identified as a putative biomarker of major depressive disorder. Accumulating evidence have repeatedly shown reduced PFC GBCr in major depressive disorder, an abnormality that appears to normalize following ketamine treatment. Methods Fifty-six unmedicated participants with major depressive disorder were randomized to intravenous placebo (normal saline; n = 18), ketamine (0.5 mg/kg; n = 19), or lanicemine (100 mg; n = 19). PFC GBCr was computed using time series from functional magnetic resonance imaging scans that were completed at baseline, during infusion, and at 24-h posttreatment. Results Compared to placebo, ketamine significantly increased average PFC GBCr during infusion ( p = 0.01) and at 24-h posttreatment ( p = 0.02). Lanicemine had no significant effects on GBCr during infusion ( p = 0.45) and at 24-h posttreatment ( p = 0.23) compared to placebo. Average delta PFC GBCr (during minus baseline) showed a pattern of positively predicting depression improvement in participants receiving ketamine ( r = 0.44; p = 0.06; d = 1.0) or lanicemine ( r = 0.55; p = 0.01; d = 1.3) but not those receiving placebo ( r = −0.1; p = 0.69; d = 0.02). Follow-up vertex-wise analyses showed ketamine-induced GBCr increases in the dorsolateral, dorsomedial, and frontomedial PFC during infusion and in the dorsolateral and dorsomedial PFC at 24-h posttreatment ( corrected p < 0.05). Exploratory vertex-wise analyses examining the relationship with depression improvement showed positive correlation with GBCr in the dorsal PFC during infusion and at 24-h posttreatment but negative correlation with GBCr in the ventral PFC during infusion ( uncorrected p < 0.01). Conclusions In a randomized placebo-controlled approach, the results provide the first evidence in major depressive disorder of ketamine-induced increases in PFC GBCr during infusion and suggest that ketamine’s rapid-acting antidepressant properties are related to its acute effects on prefrontal connectivity. Overall, the study findings underscore the similarity and differences between ketamine and another N-methyl-D-aspartate receptor antagonist while proposing a pharmacoimaging paradigm for the optimization of novel rapid-acting antidepressants prior to testing in costly clinical trials.

scholarly journals Identification of Core Genes and Pathways in Major Depressive Disorder Applying Bioinformatics

2020 ◽  
Author(s):  
Wenshan Yang ◽  
Hong Yin ◽  
Yichen Wang ◽  
Ping Liu ◽  
Yuan Hu
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Signaling Pathway ◽  
Kegg Pathway ◽  
Enrichment Analysis ◽  
Ppi Network ◽  
Biological Mechanisms ◽  
Major Depressive ◽  
Kegg Pathway Analysis ◽  
Depressive Patients

Abstract Background: Although extensive study efforts on major depressive disorder (MDD), the pathogenesis related to the biological factors are not fully understood and present therapeutic regimen are ineffective in some depressive patients. This study aims to identify key genes and pathways associated with the molecular biological mechanisms of major depressive disorder through bioinformatics analysis in the Gene Expression Omnibus (GEO) public database of the National Center for Biotechnology Information (NCBI) website.Materials and methods: The whole-transcriptome brain expression profile dataset (GSE101521) was obtained from the GEO database. Differentially-expressed genes (DEGs) in normal group (non-psychiatric human) and MDD group (depressive patients) were identified applying Networkanalyst online database. Gene ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were performed to function annotation and enrichment analysis. After that, STRING online database was conducted to protein–protein interaction (PPI) network, and Cytoscape.3.7.2 software was performed to module analysis. Results: Out of the 41 DEGs identified from normal tissue samples and MDD, 39 were upregulated and 2 were downregulated. GO enrichment analysis discovered that DEGs were primarily involved in inflammatory response, and KEGG pathway analysis suggested that the most chiefly pathway related to MDD were IL-17 signaling pathway, TNF signaling pathway and NOD-like receptor signaling pathway. Six hub genes (IL6, CXCL8, IL1B, FOS, CCL2 and CXCL2) were identified by PPI network and module analysis. Conclusion: Our current study detected novel markers and targets involved immune system, which are involved in pivotal biological mechanisms related to the pathogenesis of major depression. Looking forward, these findings still need to be validated in future experimental studies.

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