Expression data of the Cerebral cortex in Tyr-Trp treated AD model mouse
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA610506 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Scope: As a result of population ageing, the number of Alzheimer’s disease (AD) patients has rapidly increased. There are many hypothesises on the pathogenesis of AD, but its detailed molecular mechanism is still unknown, and so no effective preventive or therapeutic measures have been established. Some reports showed a decrease in levels of norepinephrine (NE) has been suspected to be involved in the decline of cognitive function in AD patients and NE concentrations were decreased in postmortem AD patient brains. Tyr-Trp was identified as being the most effective dipeptide in enhancing norepinephrine (NE) synthesis and metabolism. And Tyr-Trp treatment ameliorated the short-term memory dysfunction in AD model mice caused by amyloid beta (Aβ) 25-35. So, the purpose of this study was to investigate the preventive or/and protective effects of Tyr-Trp administration in AD model mice. Methods and results: ddY mice were fed normal diet. After 7 days of feeding, mice were divided into 3 groups (n=10 per group) as follows: the sham group, which received saline administration and distilled water injection; the Aβ group, which received saline administration and Aβ peptides 25–35 injection; and the Aβ+YW group, which received Tyr-Trp administration and Aβ peptides 25–35 injection. Tyr-Trp was orally administered Tyr-Trp (100 mg kg-1 day-1, twice a day), starting 7 days before Aβ peptides injection. The other groups received oral administration of saline (5 mL kg-1). After Aβ peptides injection or sham operation, each groups received every oral administration. DAN microarray showed that Tyrosine hydroxylase, dopa decarboxylase and dopamine receptor D2 mRNA expressions which were downregulated in Aβ group comparing with sham group were upregulated in Aβ+YW group comparing with Aβ group. In addition, quinoid dihydropteridine reductase mRNA expression which wasn’t changed in Aβ group comparing with sham group was upregulated in Aβ+YW group comparing with Aβ group. Conclusions: These results suggest that Tyr-Trp administration might ameliorate the short-term memory dysfunction in AD model mice because of enhancing norepinephrine (NE) synthesis and metabolism through metabolism of both Tyr and Trp.
2020-04-30 | GSE146400 | GEO
Project description:Transient receptor potential (TRP) ion channels are polymodal cation channels with well-established roles in peripheral sensory systems, whereas their expression landscape in the adult cerebral cortex remains incompletely defined. This study provides integrated Oxford Nanopore direct RNA sequencing and Illumina RNA-seq datasets from adult mouse cortex, together with Illumina RNA-seq of dorsal root ganglia as a peripheral sensory reference. Three independent cortical biological replicates were profiled on both platforms. These datasets enable quantitative analysis of TRP channel gene- and isoform-level expression, cross-platform comparison of transcript abundance, and full-length transcript characterisation using long-read sequencing aligned to the Ensembl GRCm39 release 115 reference genome. Raw sequencing files and processed gene- and transcript-level expression tables are provided as a resource for transcriptomic analysis of adult mouse neural tissues.
2026-04-10 | GSE315051 | GEO
Project description:The prevalence of glioblastoma increases with age. Advanced age is also one of the best-established risk factors for sporadic Alzheimer's disease (AD). Previous histopathological studies detected the occurrence of AD features in frontal cortex specimens from glioblastoma patients. This study aimed to identify AD-related transcript changes in cerebral cortex specimens obtained during surgery for glioblastoma. The study analyzed cerebral cortex specimens from three groups of glioblastoma patients (Group1, Group2, Group3). The transcriptome study of this Group1 includes specimens from 10 glioblastoma patients (Patient1-Patient10).
2026-02-16 | GSE318045 | GEO
Project description:Differential gene expression of cerebral cortex might be responsible for distinct neurovascular developments between different mouse strains We used Affymetrix microarray to explore the global gene expression patterns of mouse cerebral cortex of different mouse strains at two developmental stages Cerebral cortex from two mouse strains [C57BL/6J(B6) and C3H/J (C3H)] at post-natal day 1 (p1) and post-natal 11 weeks (11 wk) were harvested for microarray experiments
2013-10-21 | E-GEOD-46443 | biostudies-arrayexpress
Project description:<p><strong>BACKGROUND:</strong> The protozoan parasite Toxoplasma gondii infects and alters the neurotransmission in cerebral cortex and other brain regions, leading to neurobehavioral and neuropathologic changes in humans and animals. However, the molecules that contribute to these changes remain largely unknown.</p><p><strong>METHODS:</strong> We have investigated the impact of T. gondii infection on the overall metabolism of mouse cerebral cortex. Mass-spectrometry-based metabolomics and multivariate statistical analysis were employed to discover metabolomic signatures that discriminate between cerebral cortex of T. gondii-infected and uninfected control mice.</p><p><strong>RESULTS:</strong> Our results identified 73, 67 and 276 differentially abundant metabolites, which were involved in 25, 37 and 64 pathways at 7, 14 and 21 days post-infection (dpi), respectively. Metabolites in the unsaturated fatty acid biosynthesis pathway were upregulated as the infection progressed, indicating that T. gondii induces the biosynthesis of unsaturated fatty acids to promote its own growth and survival. Some of the downregulated metabolites were related to pathways, such as steroid hormone biosynthesis and arachidonic acid metabolism. Nine metabolites were identified as T. gondii responsive metabolites, namely galactosylsphingosine, arachidonic acid, LysoSM(d18:1), L-palmitoylcarnitine, calcitetrol, 27-Deoxy-5b-cyprinol, L-homophenylalanine, oleic acid and ceramide (d18:1/16:0).</p><p><strong>CONCLUSIONS:</strong> Our data provide novel insight into the dysregulation of the metabolism of the mouse cerebral cortex during T. gondii infection and have important implications for studies of T. gondii pathogenesis.</p>
2020-04-23 | MTBLS770 | MetaboLights
Project description:Differential gene expression of cerebral cortex might be responsible for distinct neurovascular developments between different mouse strains We used Affymetrix microarray to explore the global gene expression patterns of mouse cerebral cortex of different mouse strains at two developmental stages
2013-10-21 | GSE46443 | GEO
Project description:Expression data from mouse cerebral cortex
| PRJNA508404 | ENA
Project description:This SuperSeries is composed of the following subset Series: GSE27459: Human cerebral cortex DNA methylation by MeDIP-Chip GSE27460: Rhesus macaque cerebral cortex DNA methylation profiling by MeDIP-Chip Refer to individual Series
2012-03-01 | E-GEOD-27461 | biostudies-arrayexpress
Project description:Cajal-Retzius cells have important role in cerebral cortex development, such as secreted Reln protein, maintain normal lays of cerebral cortex. To explore novel secretory protein of Cajal-Retzius cells and to survey the roles of Cajal-Retzius cells in cerebral cortex development, we analyzed transcriptome profiles of 6753 single cells of the embryonic 18 days.
2019-11-27 | GSE123035 | GEO
Project description:Thiele2013 - Cerebral cortex neuronal cells
The model of cerebral cortex neuronal cells metabolism is derived from the community-driven global reconstruction of human metabolism (version 2.02, MODEL1109130000
).
This model is described in the article:
A community-driven global reconstruction of human metabolism.
Thiele I, et al
.
Nature Biotechnology
Abstract:
Multiple models of human metabolism have been reconstructed, but each represents only a subset of our knowledge. Here we describe Recon 2, a community-driven,
consensus 'metabolic reconstruction', which is the most comprehensive representation of human metabolism that is applicable to computational modeling. Compared
with its predecessors, the reconstruction has improved topological and functional features, including ~2x more reactions and ~1.7x more unique metabolites. Using
Recon 2 we predicted changes in metabolite biomarkers for 49 inborn errors of metabolism with 77% accuracy when compared to experimental data. Mapping metabolomic
data and drug information onto Recon 2 demonstrates its potential for integrating and analyzing diverse data types. Using protein expression data, we automatically
generated a compendium of 65 cell type-specific models, providing a basis for manual curation or investigation of cell-specific metabolic properties. Recon 2 will
facilitate many future biomedical studies and is freely available at http://humanmetabolism.org/.
This model is hosted on BioModels Database
and identified by: MODEL1310110033
.
To cite BioModels Database, please use: BioModels Database: An enhanced,
curated and annotated resource for published quantitative kinetic models
.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer
to CC0 Public Domain Dedication
for more information.
2005-01-01 | MODEL1310110033 | BioModels