Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1236379 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR32701636_1.fastq.gz | Fastqsanger.gz | |||
| SRR32701636_2.fastq.gz | Fastqsanger.gz | |||
| SRR32701637_1.fastq.gz | Fastqsanger.gz | |||
| SRR32701637_2.fastq.gz | Fastqsanger.gz | |||
| SRR32701638_1.fastq.gz | Fastqsanger.gz |
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Project description:Early-life gut microbiome maturity regulates blood-brain barrier and cognitive development
| PRJNA1232707 | ENA
Project description:The gut microbiome is an emerging factor in the neurobiology of disease. Blood-brain barrier (BBB) integrity is essential for proper brain function. However, the role the initial microbiome plays in BBB and brain development is unclear. In this study, we colonized germ-free pregnant mice with human full-term- or preterm-infant-derived gut microbiota, thereby establishing these communities in the resulting offspring. We discovered that mice harboring a full-term-associated microbiome exhibited stronger memory and learning capabilities and dramatically decreased early-life BBB permeability when compared to those with a prematurity-associated microbiome. Whole-brain single-cell RNA sequencing revealed downregulation of synaptic signaling genes in BBB cell types of mice with the prematurity-associated microbiome, indicating that microbiome maturity influences BBB transcriptional programs that support cognitive development. Comprehensive metagenomics and metabolomics uncovered bacterial populations and genomic pathways corresponding with decreased levels of circulating long-chain acylcarnitines and lysophosphatidylcholines in mice with the full-term-associated microbiome. Our findings highlight the microbiome as a therapeutic target for improving long-term neurodevelopmental outcomes due to its effect on the early-life BBB.
2025-08-18 | GSE291278 | GEO
Project description:Blood collected from infants at week 6 and week 7 of life to profile how the transcriptome is changed following routine early life vaccination. Paired faecal metagenomic data is available for these infants under BioProject PRJNA807448 at the Sequence Read Archive.
2025-01-14 | GSE198276 | GEO
Project description:we developed a novel brain-penetrant inhibitor of G9a, MS1262, across the blood-brain barrier to block this G9a-regulated, proteopathologic mechanism. Intermittent MS1262 treatment of multiple AD mouse models consistently restored both cognitive and noncognitive functions to healthy levels. Comparison of proteomic/phosphoproteomic analyses of MS1262-treated AD mice with human AD patient data identified multiple pathological brain pathways that elaborate amyloid beta and neurofibrillary tangles as well as blood coagulation, from which biomarkers of early stage of AD including SMOC1 were found to be affected by MS1262 treatment.
2025-03-18 | PXD047045 | Pride
Project description:<p>Background: Chronic use of antipsychotic drugs is associated with neuronal damage and cognitive impairment, potentially mediated by alterations in gut microbiota metabolites, although the specific metabolite involved remains unknown.</p><p>Objective: To identify the key metabolite responsible for antipsychotic-induced synaptic and cognitive impairment and assess the potential for its reversal through targeted supplementation.</p><p>Design: Mice were chronically treated (8 weeks) with olanzapine, risperidone, or clozapine. In the olanzapine model, gut microbiota (16S rRNA and shotgun metagenomic sequencing) and metabolites (untargeted metabolomics) were analyzed, identifying ergothioneine depletion, validated in olanzapine-treated patients. Causality was tested via fecal microbiota transplantation (FMT) and ergothioneine supplementation. Neuronal-specific PTP1B knockout mice elucidated mechanistic pathways.</p><p>Results: Chronic olanzapine treatment caused gut microbial dysbiosis, disrupted intestinal barrier integrity, and impaired cognitive function in mice. A key finding was the depletion of ergothioneine, the gut microbiota-derived metabolite, in both the blood and brain of mice, and in the blood of patients receiving olanzapine. This depletion was associated with a loss of ergothioneine-producing Cyanobacteria and subordinate taxa. Similar ergothioneine depletion and cognitive impairments were observed in risperidone- and clozapine-treated mice. Ergothioneine supplementation or FMT effectively prevented olanzapine-induced cognitive and synaptic impairments. Mechanistically, ergothioneine attenuated olanzapine-induced hippocampal oxidative stress and inhibited the redox-sensitive phosphatase PTP1B. Furthermore, neuronal- or hippocampal neuronal-specific deletion of PTP1B abolished olanzapine-induced synaptic and cognitive impairments. </p><p>Conclusions: The significant reduction of ergothioneine induced by antipsychotic treatment leads to cognitive impairment, highlighting gut microbiota-derived metabolites as potential therapeutic targets for improving cognitive function in patients undergoing antipsychotic therapy.</p>
2026-04-08 | MTBLS12751 | MetaboLights
Project description:The Blood-Brain Barrier (BBB) is a crucial, selective barrier that regulates the entry of molecules including nutrients, environmental toxins, and therapeutic medications into the brain. This function relies heavily on brain endothelial cell proteins, particularly transporters and tight junction proteins. The BBB continues to develop postnatally, adapting its selective barrier function across different developmental phases, and alters with aging and disease. Here we present a global proteomics analysis focused on the ontogeny and aging of proteins in human brain microvessels (BMVs), predominantly composed of brain endothelial cells. Our proteomic profiling quantified 6,223 proteins and revealed possible age-related alteration in BBB permeability due to basement membrane component changes through the early developmental stage and age-dependent changes in transporter expression. Notable changes in expression levels were observed with development and age in nutrient transporters and transporters that play critical roles in drug disposition. This research 1) provides important information on the mechanisms that drive changes in the metabolic content of the brain with age and 2) enables the creation of physiologically based pharmacokinetic models for CNS drug distribution across different life stages.
2025-11-28 | PXD057192 | Pride
Project description:We applied metagenomic shotgun sequencing to investigate the effects of ZEA exposure on the change of mouse gut microbiota composition and function.
2019-11-09 | GSE140149 | GEO
Project description:Background: Cadmium (Cd) is a heavy metal recognized as a neurotoxicant. However, the mechanisms underlying its neurotoxicity remain poorly understood. The gut-brain axis, a bidirectional communication pathway between the central nervous system and the gut microbiome, has been linked to various neurological disorders. Because the gut microbiome is a known target of Cd, it is important to investigate whether the gut-brain axis mechanistically contributes to the Cd-induced neurotoxicity. Objective: In our initial exploration of the role of the gut-brain axis in modulating Cd neurotoxicity on cognition, we investigated whether Cd exposure induces gut dysbiosis before the onset of cognitive deficits and explored the potential link between gut microbiome alterations and Cd-induced cognitive deficits. Methods: Adult male mice were exposed to 3 mg/L Cd via drinking water for nine weeks. Behavioral assessments were conducted throughout the exposure period to evaluate cognitive function. Fresh fecal pellets were collected weekly to monitor gut microbiome composition. The effects of Cd on the hippocampus and intestine were analyzed using transcriptomics and mass spectrometry (MS)-based metabolomics. Results: Cd exposure resulted in hippocampus-dependent learning and memory deficits, first observed at four weeks into exposure. RNA sequencing of the hippocampus at the terminal time point revealed reduced expression of genes involved in cognition and neuroinflammation in Cd exposed mice. Metagenomic shotgun sequencing showed that Cd-induced gut dysbiosis preceded the onset of cognitive impairments, with specific bacterial species associated with Cd-induced cognitive deficits, confirmed by using the cor.test function (Spearman correlation, p < 0.1) in R. Furthermore, Cd exposure compromised intestinal barrier integrity, increased inflammatory cytokines levels, and altered the levels of neuroactive microbial metabolites in mice, which may be linked to Cd-induced gut dysbiosis Conclusion: Our study is the first to show that Cd exposure triggers gut microbial shifts before the onset of cognitive deficits, accompanied by increased intestinal permeability and elevated proinflammatory biomarkers in both the intestine and brain at the terminal time point. These findings suggest a potential critical role of gut-brain axis in modulating Cd neurotoxicity and underscore the need for future research to elucidate the mechanistic involvement of gut microbiome as a potential target for mitigating Cd-induced cognitive decline.
2026-04-01 | GSE293538 | GEO
Project description:Metagenomic signatures of early life brain damage
| PRJNA1112760 | ENA
Project description:The antagonistic pleiotropy theory of aging predicts genetic trade-offs between early-life and late-life fitness. However, empirical evidence for these trade-offs in vertebrates remains scarce, particularly in the context of ecologically relevant life histories. Here, we identify vestigial-like 3 (vgll3), a transcription cofactor previously linked with age at maturity in humans and Atlantic salmon through GWAS studies, as an antagonistically pleiotropic gene in turquoise killifish (Nothobranchius furzeri). By disrupting two conserved vgll3 isoforms, we show that reduction of vgll3, in an isoform- or dose-dependent manner, accelerated male growth and reproductive development. This indicates that vgll3 regulates male sexual maturity. However, early-life benefits come at a late-life cost, as older mutant males with a disrupted long isoform develop melanoma-like tumors, validated via transplantation into immunodeficient rag2 models, and exhibit increased age-related mortality rate. These findings highlight vgll3 as a key regulator of vertebrate life-history trade-offs, balancing early-life fitness with late-life disease risks.
2026-04-10 | GSE300596 | GEO