Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12960941_1.fastq.gz | Fastqsanger.gz | |||
| SRR12960941_2.fastq.gz | Fastqsanger.gz | |||
| SRR12960942_1.fastq.gz | Fastqsanger.gz | |||
| SRR12960942_2.fastq.gz | Fastqsanger.gz | |||
| SRR12960943_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Social anxiety disorder (SAD) is a psychiatric disorder characterized by severe fear in social situations and avoidance of these. Multiple genetic as well as environmental factors contribute to the etiopathology of SAD. One of the main risk factors for SAD is stress, especially during early periods of life (early life adversity; ELA). ELA leads to structural and regulatory alterations contributing to disease vulnerability. This includes the dysregulation of the immune response. However, the molecular link between ELA and the risk for SAD in adulthood remain largely unclear. Evidence is emerging that long-lasting changes of gene expression patterns play an important role in the biological mechanisms linking ELA and SAD. Therefore, we conducted a transcriptome study of SAD and ELA performing RNA sequencing in peripheral blood samples. Analyzing differential gene expression between individuals suffering from SAD with high or low levels of ELA and healthy individuals with high or low levels of ELA, 13 significantly differentially expressed genes (DEGs) were identified with respect to SAD whilst no significant differences in expression were identified with respect to ELA. The most significantly expressed gene was MAPK3 (p=0.003) being upregulated in the SAD group compared to control individuals. In contrary, weighted gene co-expression network analyses (WGCNA) identified only modules significantly associated with ELA (p≤0.05), not with SAD. Furthermore, analyzing interaction networks of the genes from the ELA-associated modules and the SAD-related MAPK3) revealed complex interactions of those genes. Gene functional enrichment analyses indicate a role of signal transduction pathways as well as inflammatory responses supporting an involvement of the immune system in the association of ELA and SAD. In conclusion, we did not identify a direct molecular link between ELA and adult SAD by transcriptional changes. However, our data indicate an indirect association of ELA and SAD mediated by the interaction of genes involved in immune-related signal transduction.
2023-04-16 | GSE228702 | GEO
Project description:Social anxiety disorder (SAD) is a psychiatric disorder characterized by extensive fear in social situations. Multiple genetic and environmental factors are known to contribute to its pathogenesis. One of the main environmental risk factors is early life adversity (ELA). Evidence is emerging that epigenetic mechanisms such as DNA methylation might play an important role in the biological mechanisms underlying SAD and ELA. To investigate the relationship between ELA, DNA methylation, and SAD, we performed an epigenome-wide association study for SAD and ELA examining DNA from whole blood of a cohort of 143 individuals using DNA methylation arrays. We identified two differentially methylated regions (DMRs) associated with SAD located within the genes SLC43A2 and TNXB. As this was the first epigenome-wide association study for SAD, it is worth noting that both genes have previously been associated with panic disorder. Further, we identified two DMRs associated with ELA within the SLC17A3 promoter region and the SIAH3 gene and several DMRs that were associated with the interaction of SAD and ELA. Of these, the regions within C2CD2L and MRPL28 showed the largest difference in DNA methylation. Lastly, we found that two DMRs were associated with both the severity of social anxiety and ELA, however, neither of them was found to mediate the contribution of ELA to SAD later in life. Future studies are needed to replicate our findings in independent cohorts and to investigate the biological pathways underlying these effects.
2021-01-31 | GSE164056 | GEO
Project description:Mesenchymal stromal cells from adipose tissue (AD-MSCs) exhibit favourable clinical traits for autologous transplantation and can develop a ‘Schwann-like’ phenotype (sAD-MSCs) to improve peripheral nerve regeneration, where severe injuries yield insufficient recovery. However, sAD-MSCs regress without biochemical stimulation and detach from conduits under unfavourable transplant conditions, negating their paracrine effects. Graphene-derived materials support AD-MSC attachment, regulating cell adhesion and function through physiochemistry and topography. We report graphene oxide (GO) as a suitable substrate for human sAD-MSCs incubation towards severe peripheral nerve injuries, through evaluating transcriptome changes, neurotrophic factor expression over a 7-day period, and cell viability in apoptotic conditions. Transcriptome changes from GO incubation across four patients were minor compared to biological variance.
2021-03-08 | E-MTAB-10078 | biostudies-arrayexpress
Project description:Although sporadic AD (sAD) accounts for the majority of AD cases, the underlying mechanisms remain largely unknown. Here we modeled sAD using human induced pluripotent stem cell (iPSC)-derived three-dimensional brain organoids. We exposed brain organoids to serum to mimic the serum exposure consequence of BBB breakdown in AD patient brains. The serum-exposed brain organoids were able to recapitulate AD-like pathologies, including increased Aβ aggregates and p-Tau level, synaptic loss, and impaired calcium signaling and neural network. Serum exposure increased Aβ and p-Tau levels through inducing BACE and GSK3α/β levels, respectively. In addition, single-cell transcriptomic analysis of brain organoids revealed that serum exposure reduced synaptic function in both neurons and astrocytes, and induced immune response in astrocytes. The human brain organoid-based sAD model established in this study could provide a powerful platform for both mechanistic study and therapeutic development.
2021-09-29 | GSE164089 | GEO
Project description:Evidence suggests that extracellular vesicles (EVs) act as mediators and biomarkers of neurodegenerative diseases. Two distinct forms of Alzheimer Disease (AD) are known: a late-onset sporadic form (SAD) and an early-onset familial form (FAD). This project aims to characterize and compare the protein profile of systemic EVs from postmortem SAD and FAD patients and compared them to postmortem controls. We used LC-MS/MS label-free analysis.
2021-09-09 | PXD021718 | Pride
Project description:C. elegans SAD-1 kinase in vitro phosphorylation of SYD-2.
2023-03-10 | MSV000091471 | MassIVE