Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8334560_1.fastq.gz | Fastqsanger.gz | |||
| SRR8334560_2.fastq.gz | Fastqsanger.gz | |||
| SRR8334570_1.fastq.gz | Fastqsanger.gz | |||
| SRR8334570_2.fastq.gz | Fastqsanger.gz | |||
| SRR8334561_1.fastq.gz | Fastqsanger.gz |
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Project description:In this study, we intend to focus on pathologically diagnosed alcohol dependence patients and select isotope-labeling-based high-resolution protein quantitative The study will focus on patients with alcohol dependence and their rehabilitation treatment, through proteomic studies at the peripheral blood level and quantitative validation at the clinical level, to clarify the relationship between alcohol dependence and the regulation of protein expression in the body, and to identify the biomarkers. Through proteomics research at the peripheral blood level and quantitative validation at the clinical level, the relationship between alcohol dependence and the regulation of protein expression in the body will be clarified, and biomarkers will be identified to explore the molecular mechanism and early warning of alcohol dependence. We will also identify biomarkers and explore the molecular mechanism of alcohol dependence, as well as early warning indicators and auxiliary diagnostic indicators.
| PXD064357 |
Project description:<p>This study includes SSADDA (Semi Structured Assessment for Drug Dependence and Alcoholism) assessed subjects (mostly unrelated, but including some affected sibling pairs) recruited in the course of several substance dependence genetics projects. The sample includes 1889 African-American (AA) subjects and 1020 European-American (EA) subjects. Among the AAs, 1397 meet DSM-IV criteria for alcohol dependence and 491 are controls. Among the EAs, 1010 meet the criteria for alcohol dependence and 9 are controls. (One in each population meets criteria for alcohol abuse and not dependence, and is therefore counted in neither category.) Although alcohol dependence is the major focus, the sample is informative also for cocaine, nicotine, and opioid dependence.</p>
| phs000425.v1.p1 | EGA
Project description:Purpose: Alcohol dependence results in microglia proliferation in brain and changes in microglia morphology and function. However, it remains unknown if microglia initiate or simply amplify the neuroadaptations that lead to alcohol dependence. Here we determined microglia function in chronic intermittent ethanol exposure behaviors using a colony stimulating factor 1 receptor inhibitor (PLX5622) and 3’UTR biased-sequencing. Therefore, the purpose of this study was to provide insight into how microglia may regulate neuroadaptations due to alcohol dependence. Methods: We performed 3’UTR biased transcriptome sequencing (3’Tag-seq) on total homogenate isolated from the prefrontal cortex (PFC) and central nucleus of the amygdala (CeA) of C57BL6/J mice following microglia depletion and chronic intermittent ethanol exposure. Results: Differential expression analysis and WGCNA network analysis revealed that microglia depletion prevents both immune and synaptic gene expression changes that are linked with the formation of alcohol dependence. This suggested that microglia are key regulators of the transition from alcohol misuse to alcohol dependence. Conclusion: Taken together our behavioral and transcriptional data indicate that microglia are the primary effector cell responsible for regulation of alcohol dependence. In addition, our data represents a novel resource for groups interested in transcriptional effects of microglia depletion after alcohol dependence.
2020-11-27 | GSE142571 | GEO
Project description:The prefrontal cortex is a crucial regulator of escalation of alcohol drinking, dependence, and other behavioral criteria associated with AUD. Comprehensive identification of cell-type specific transcriptomic changes in alcohol dependence will improve our understanding of mechanisms mediating the escalation of alcohol use and will refine targets for therapeutic development. We performed single nucleus RNA sequencing (snRNA-seq) on ~150,000 single nuclei from the medial prefrontal cortex (mPFC) obtained from C57BL/6J mice exposed to the chronic intermittent ethanol exposure (CIE) paradigm which models phenotypes associated with alcohol dependence. Gene co-expression network analysis and differential expression analysis identified highly dysregulated co-expression networks in multiple cell types. Here, we present a comprehensive atlas of cell-type specific alcohol dependence related gene expression changes in the mPFC.
2024-01-10 | GSE233763 | GEO
Project description:Hemorphins are short peptides generated during cleavage of the hemoglobin chains but alpha chain, with various functions in different systems and tissues in both physiology and pathophysiology. The main purpose of this study was to establish the role of LVV-H7 in the mechanism of alcohol dependence. LVV-hemorphin 7 (LVV-H7) is released at higher concentrations in the presence of alcohol in vitro. Therefore, we predicted that alcohol intake can change the level of LVV-H7. We have accomplished behavioral tests in animal studies, along with proteomic analysis of the CNS tissues of alcohol addicted rats to verify the correlation of LVV-H7 level and ethanol dependence. We have also confirmed the BBB permeability of synthesized LVV-H7, as well as an inhibitor of its releasing enzyme- pepstatin using fluorescent microscopy. We have found a dose-dependent correlation between LVV-H7 and the time spent by rats in the drug-associated compartment using CPP test. Utilizing mass spectrometry-based methods we identified protein binding targets of LVV-H7 in the CNS tissue of addicted rats, along with the LVV-H7 degrading enzymes. The interpretation of the obtained results reveals the substantial role of LVV-H7 in the mechanism of alcohol dependence.
2025-09-05 | PXD036448 | Pride
Project description:Sustained or repeated exposure to sedating drugs such as alcohol triggers homeostatic adaptations in the brain that lead to the development of drug tolerance and dependence. These adaptations involve long-term changes in the transcription of drug-responsive genes as well as an epigenetic restructuring of chromosomal regions that is thought to signal and maintain the altered transcriptional state. Drug-induced epigenetic changes have been shown to be important in the long-term adaptation that leads to alcohol tolerance and dependence endophenotypes. A major constraint impeding progress is that alcohol produces a surfeit of changes in gene expression, most that may not make any meaningful contribution to the ethanol response under study. Here we used a novel genomic epigenetic approach to find genes relevant for functional alcohol tolerance by exploiting the commonalities of two chemically distinct drugs. In Drosophila melanogaster, ethanol and benzyl alcohol induce mutual cross-tolerance, indicating that they share a common mechanism for producing tolerance. We surveyed the genome-wide changes in histone acetylation that occur in response to these drugs. Each drug induces modifications in a large number of genes. The genes that respond similarly to either treatment, however, represent a subgroup enriched for genes important for the common tolerance response. Genes were functionally tested for behavioral tolerance to the sedative effects of ethanol and benzyl alcohol using mutant and inducible RNAi stocks. We identified a network of genes that are essential for the development of tolerance to sedation by alcohol.
2013-09-05 | GSE48449 | GEO
Project description:We analyzed cerebral cortices (CTX) and midbrains (MB) from male C57BL/6J mice subjected to a CIE, 2BC paradigm, which induces heavy drinking and represents one of the best available animal models for alcohol dependence and relapse drinking.
2013-12-31 | GSE48576 | GEO