scholarly journals Brain transcriptome responses to dexamethasone depending on dose and sex reveal factors contributing to sex-specific vulnerability to stress-induced disorders

2021 ◽  
Author(s):  
Eduard Murani ◽  
Nares Trakooljul ◽  
Frieder Hadlich ◽  
Siriluck Ponsuksili ◽  
Klaus Wimmers
2016 ◽  
Author(s):  
Paula Nelas ◽  
Diana Gandara ◽  
Cláudia Chaves ◽  
Emília Coutinho ◽  
Carla Cruz ◽  
...  

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Hui Yung Chin ◽  
Michael Lardelli ◽  
Lyndsey Collins-Praino ◽  
Karissa Barthelson

AbstractMutation of the gene PARK7 (DJ1) causes monogenic autosomal recessive Parkinson’s disease (PD) in humans. Subsequent alterations of PARK7 protein function lead to mitochondrial dysfunction, a major element in PD pathology. Homozygous mutants for the PARK7-orthologous genes in zebrafish, park7, show changes to gene expression in the oxidative phosphorylation pathway, supporting that disruption of energy production is a key feature of neurodegeneration in PD. Iron is critical for normal mitochondrial function, and we have previously used bioinformatic analysis of IRE-bearing transcripts in brain transcriptomes to find evidence supporting the existence of iron dyshomeostasis in Alzheimer’s disease. Here, we analysed IRE-bearing transcripts in the transcriptome data from homozygous park7−/− mutant zebrafish brains. We found that the set of genes with “high quality” IREs in their 5′ untranslated regions (UTRs, the HQ5′IRE gene set) was significantly altered in these 4-month-old park7−/− brains. However, sets of genes with IREs in their 3′ UTRs appeared unaffected. The effects on HQ5′IRE genes are possibly driven by iron dyshomeostasis and/or oxidative stress, but illuminate the existence of currently unknown mechanisms with differential overall effects on 5′ and 3′ IREs.


2020 ◽  
Vol 7 (1) ◽  
Author(s):  
Tiziano Flati ◽  
Silvia Gioiosa ◽  
Giovanni Chillemi ◽  
Andrea Mele ◽  
Alberto Oliverio ◽  
...  

AbstractStressful experiences are part of everyday life and animals have evolved physiological and behavioral responses aimed at coping with stress and maintaining homeostasis. However, repeated or intense stress can induce maladaptive reactions leading to behavioral disorders. Adaptations in the brain, mediated by changes in gene expression, have a crucial role in the stress response. Recent years have seen a tremendous increase in studies on the transcriptional effects of stress. The input raw data are freely available from public repositories and represent a wealth of information for further global and integrative retrospective analyses. We downloaded from the Sequence Read Archive 751 samples (SRA-experiments), from 18 independent BioProjects studying the effects of different stressors on the brain transcriptome in mice. We performed a massive bioinformatics re-analysis applying a single, standardized pipeline for computing differential gene expression. This data mining allowed the identification of novel candidate stress-related genes and specific signatures associated with different stress conditions. The large amount of computational results produced was systematized in the interactive “Stress Mice Portal”.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Céline H. De Jager ◽  
Charles C. White ◽  
David A. Bennett ◽  
Yiyi Ma

AbstractAccumulating evidence has suggested that the molecular transcriptional mechanism contributes to Alzheimer’s disease (AD) and its endophenotypes of cognitive decline and neuropathological traits, β-amyloid (Aβ) and phosphorylated tangles (TAU). However, it is unknown what is the impact of the AD risk factors, personality characteristics assessed by the NEO Five-Factor Inventory, on the human brain’s transcriptome. Using postmortem human brain samples from 466 subjects, we found that neuroticism has a significant overall impact on the brain transcriptome (omnibus P = 0.005) but not the other four personality characteristics. Focused on those cognitive decline related gene co-expressed modules, neuroticism has nominally significant associations (P < 0.05) with four neuronal modules, which are more related to PHFtau than Aβ across all eight brain regions. Furthermore, the effect of neuroticism on cognitive decline and AD might be mediated through the expression of module 7 and TAU pathology (P = 0.008). To conclude, neuroticism has a broad impact on the transcriptome of human brains, and its effect on cognitive decline and AD may be mediated through gene transcription programs related to TAU pathology.


2017 ◽  
Vol 66 (3) ◽  
pp. 186-198 ◽  
Author(s):  
Bachaer Ayed ◽  
Ikram Jmal ◽  
Samir Sahal ◽  
Fatma Ben Brahim ◽  
Emna Boughariou ◽  
...  

2021 ◽  
pp. 111451
Author(s):  
Alyssa N. Cavalier ◽  
Zachary S. Clayton ◽  
David A. Hutton ◽  
Devin Wahl ◽  
Julie A. Reisz ◽  
...  

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