Predictors of depression in breast cancer patients during and after radiotherapy: Role of chemotherapy and the inflammatory response
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE41112 | GEO | 2013/01/01
SECONDARY ACCESSION(S): PRJNA178359
REPOSITORIES: GEO
Similar Datasets
Project description:Chemotherapy and the inflammatory response were associated with persistent depressive symptoms in breast cancer patients undergoing radiation. Treatments targeting inflammation before radiation may reduce depression post radiation therapy, especially in patients who have been treated previously with chemotherapy. Total RNA was isolated from the peripheral blood mononuclear cells (PBMC) obtained from the women (n=61) with Stage 0-III breast cancer treated with or without chemotherapy.
2013-01-01 | E-GEOD-41112 | biostudies-arrayexpress
Project description:Analysis of genes and pathways related to psychomotor retardation symptoms in patients with major depressive disorder. Results indicate that psychomotor slowing is associated with enrichment of inflammatory and metabolic pathways in unmedicated patients with depression.
2020-08-19 | GSE135524 | GEO
Project description:Depression is a complex and heterogeneous disorder and a leading contributor to the global burden of of disease. Most previous research has focused on individual brain regions and individual genes that contribute to depression. However, emerging evidence in both humans and animal models suggests that dysregulated circuit function and gene expression across multiple brain regions drive depressive phenotypes. Here we use a bioinformatics approach intersecting differential expression analysis with weighted gene co-expression network analysis to identify transcriptional networks that regulate susceptibility to depressive-like symptoms in mice. We performed RNA-sequencing on multiple brain regions from control animals and those either susceptible or resilient to chronic social defeat stress (CSDS) at multiple time points after defeat. We bioinformatically identified several transcriptional networks that regulate depression susceptibility, and in vivo manipulations of these networks confirmed their functional significance at the levels of gene transcription, synaptic regulation, and behavior. Our findings reveal novel transcriptional networks that control stress susceptibility and offer fundamentally new leads for antidepressant drug discovery.
2016-05-12 | GSE72343 | GEO
Project description:Depression is one of the most common neuropsychiatric disorders. Although the pathogenesis of depression is still unknown, environmental risk factors and genetics are implicated. Copper (Cu), a cofactor of multiple enzymes, is involved in regulating depression-related processes. Depressed patients carrying the apolipoprotein ε4 allele display more severe depressive symptoms, indicating that ApoE4 is closely associated with an increased risk of depression. The study explored the effect of low-dose Cu (0.13 ppm) exposure and ApoE4 on depression-like behavior of mice and further investigate the possible mechanisms. The 4-month-old ApoE4 mice and wild-type (WT) mice were treated with 0.13 ppm CuCl2 for 4 months. After the treatment, ApoE4 mice displayed obvious depression-like behavior compared with the WT mice, and Cu exposure further exacerbated the depression-like behavior of ApoE4 mice. There was no significant difference in anxiety behavior (Open field test) and memory behavior (Morris water maze). Proteomic analysis revealed that the differentially expressed proteins between Cu-exposed and non-exposed ApoE4 mice were mainly involved in Ras signaling pathway, protein export, axon guidance, serotonergic synapse, GABAergic synapse, dopaminergic synapse. Among these differentially expressed proteins, immune response and synaptic function are highly correlated. Representative protein expression changes are quantified by Western blot, showing consistent results as determined by proteomic analysis. Hippocampal astrocytes and microglia were increased in Cu-exposed ApoE4 mice, suggesting that neuroglial cells played an important role in the pathogenesis of depression. Taken together, our study demonstrated that Cu exposure exacerbates depression-like behavior of ApoE4 mice and the mechanisms may involve the dysregulation of synaptic function and immune response, and overactivation of neuroinflammation.
2021-09-09 | PXD022422 | Pride
Project description:The deficiency of n-3 PUFAs in the brain and depressive symptoms are closely related. Krill oil contains abundant amounts of n-3 PUFAs incorporated in phosphatidylcholine.However, the effect of krill oil treatment on depression-like behaviors induced by chronic stress and its molecular mechanism in the brain remain poorly understood. Here, we used a chronic unpredictable mild stress (CUMS) model to evaluate the effect of krill oil on depression-like behaviors and explored its molecular mechanism through lipid metabolomics and mRNA profiles in the whole brain.
2023-07-19 | GSE237760 | GEO
Project description:Several studies have suggested that SSD is a transitory phenomena in the depression spectrum and is thus considered a subtype of depression. However, the pathophysioloy of depression remain largely obscure and studies on SSD are limited. The present study compared the expression profile and made the classification with the leukocytes by using whole-genome cRNA microarrays among drug-free first-episode subjects with SSD, MDD, and healthy controls. We used microarrays to detail the global programme of gene expression to develop blood-based gene expression profiles models for classification of subsyndromal symptomatic depression and major depressive disorder
2012-03-21 | GSE32280 | GEO
Project description:<p>Depression is an individual risk factor for poor prognosis in patients with heart failure (HF). Recent studies show that gut microbiota and metabolites have critical role in comorbid HF and depressive symptoms. We recruited 95 subjects including 35 HF patients with depressive symptoms (HF-DS), 36 HF patients without depressive symptoms (HF-NDS) and 24 healthy controls (HC). The 16S rRNA, metagenome sequencing and untargeted metabolomic analysis were employed to test fecal samples. Our analysis found there was a significant difference composition of gut microbiota in HF-DS, HF-NDS and HC populations. At the genus level, Mediterranea, Tolumona and Parabacteroides were significantly increased in HF-DS patients compared with HF-NDS patients, while Pedobacter, Azospirillum and Ruminiclostridium were significantly decreased. Furthermore, anti-inflammatory mediators (abietic acid, quinic acid, linoleic acid, etc) and neurotransmitters (catechin, serotonin, tryptamine, phenylethylamine, etc) were reduced in HF-DS. The enrichment analysis revealed that the gut microbiota highly conformed with the functional pathways of metabolites, and amino acid-related metabolism, fatty acid-related metabolism and cAMP signaling pathways may be crucial biological mechanisms involved in the development of comorbid depression and HF. Finally, Cloacibacillus and alpha-tocopherol were determined as diagnostic markers for HF-DS patients.</p><p><br></p><p><strong>IMPORTANCE:</strong> There is increasing evidence that alterations in gut microbial composition and function are associated with cardiovascular or psychiatric disease. Therefore, it is meaningful to investigate the taxonomic and functional characterization of the microbiota in HF patients who also have depressive symptoms. In this cross-sectional study, Cloacibacillus and alpha-tocopherol were determined as new diagnostic markers. Furthermore, intestinal microecosystem disorders are closely linked to depressive symptoms in HF patients, providing a new reference viewpoint for understanding the gut-heart/brain axis.</p>
2023-10-23 | MTBLS8183 | MetaboLights
Project description:Recent studies implicate microglia alterations in the pathogenesis and pathophysiology of depression. For example, chronic unpredictable stress (CUS) in mice can cause degeneration of microglia and depressive-like symptoms, which can be reversed by microglia stimulating drugs. To further test the causal role of microglia in CUS-induced depression and its reversal by an anti-depressive procedure, we examined the effects of microglia depletion with the CSF-1 antagonist PLX5622 or pharmacological blockade of microglial activation with minocycline on normal mood-related behavior, CUS-induced depressive-like symptoms, and the amelioration of these symptoms by electroconvulsive treatment (ECT). We report that microglia-depleted mice showed no depression, anxiety or spatial memory disturbances. Microglia depletion had no effect on the development of CUS-induced depressive-like symptoms and suppressed neurogenesis, but it completely abrogated the beneficial effects of ECT on depression and neurogenesis, as well as on the all ECT-induced transcriptomic changes. ECT induced several morphological changes in microglia, suggestive of increased activation status, and blockade of this activation by minocycline attenuated the anti-depressive and pro-neurogenesis effect of ECT and reduced the number of contacts between microglia and neurogenic cells. The immune checkpoint gene Lag3, whose expression by microglia was increased following CUS, was the only microglial transcript significantly reduced by ECT. Furthermore, treatment of depressed-like mice with a LAG3 monoclonal antibody was further tested.
2021-01-01 | GSE123027 | GEO
Project description:Chronic stress is a major risk factor for depression, a leading cause of disability and suicide. Because current antidepressants work slowly, have common side effects, and are only effective in a minority of patients, there is an unmet need to identify the underlying molecular mechanisms. Here, we identify the receptor for neuropeptides B and W, Npbwr1, as a key regulator of depressive-like symptoms. Npbwr1 is increased in the nucleus accumbens of chronically stressed mice and postmortem in patients diagnosed with depression. Using viral-mediated gene transfer, we demonstrate a causal link between Npbwr1, dendritic spine morphology, the biomarker Bdnf, and depressive-like behaviors. Importantly, microinjection of the synthetic antagonist of Npbwr1, CYM50769, rapidly ameliorates depressive-like behavioral symptoms and alters Bdnf levels. CYM50769 is selective, well tolerated, and shows effects up to 7 days after administration of a single dose. In summary, these findings advance our understanding of mood and chronic stress and warrant further investigation of CYM50769 as a potential fast-acting antidepressant.
2024-07-05 | GSE271600 | GEO
Project description:Several studies have suggested that SSD is a transitory phenomena in the depression spectrum and is thus considered a subtype of depression. However, the pathophysioloy of depression remain largely obscure and studies on SSD are limited. The present study compared the expression profile and made the classification with the leukocytes by using whole-genome cRNA microarrays among drug-free first-episode subjects with SSD, MDD, and healthy controls. We used microarrays to detail the global programme of gene expression to develop blood-based gene expression profiles models for classification of subsyndromal symptomatic depression and major depressive disorder The present study compared the expression profile and made the classification with the leukocytes by using whole-genome cRNA microarrays among drug-free first-episode subjects with SSD, MDD, and matched controls (8 subjects in each group). Support vector machines (SVMs) were utilized for training and testing on candidate signature expression profiles from signature selection step.
2012-03-21 | E-GEOD-32280 | biostudies-arrayexpress