E-GEOD-32645
Ontology highlight
ABSTRACT:
PROVIDER: E-GEOD-32645 | ExpressionAtlas | 2025-01-24
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-32645-analysis-methods.tsv | Tabular | |||
| E-GEOD-32645-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-32645-configuration.xml | Xml | |||
| E-GEOD-32645-percentile-ranks.tsv | Tabular | |||
| E-GEOD-32645.condensed-sdrf.tsv | Tabular |
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Project description:In the present study we addressed several questions related to the mechanisms of cortical injury. We analyzed genome wide gene expression by microarrays, comparing active multiple sclerosis lesions with highly inflammatory lesions of chronic tuberculous meningitis, with neurodegenerative lesions of Alzheimer’s disease and with normal cortex of age matched controls. To clarify which inflammatory mediators drive demyelination in the human cortex, we characterized and compared the gene expression profile of cortices derived from patients with progressive Multiple Sclerosis (pMS), Meningitis tuberculosis (MT), Alzheimers disease (AD) as well as of normal cortex from age matched controls. 3 cases of each disease were included into the study. Preceding the gene expression profiling all cases were characterized histologically and areas of interest were identified. RNA was isolated from those areas, amplified and hybridized to Agilent G4112F whole genome microarrays.
2011-10-05 | E-GEOD-32645 | biostudies-arrayexpress
Project description:In the present study we addressed several questions related to the mechanisms of cortical injury. We analyzed genome wide gene expression by microarrays, comparing active multiple sclerosis lesions with highly inflammatory lesions of chronic tuberculous meningitis, with neurodegenerative lesions of Alzheimer’s disease and with normal cortex of age matched controls.
2011-10-06 | GSE32645 | GEO
Project description:Multiple sclerosis (MS) affects the cerebral cortex, inducing cortical atrophy and neuronal and synaptic pathology. Despite the fact that women are more susceptible to getting MS, men with MS have worse disability progression. Here, we address sex differences in neurodegenerative mechanisms focusing on the cerebral cortex using the MS model, chronic experimental autoimmune encephalomyelitis (EAE). RNA sequencing of neurons in cerebral cortex during EAE showed robust differential gene expression in male EAE mice compared to male healthy, age-matched, control mice. In contrast, there were few differences in female EAE mice compared to female controls. The most enriched differential gene expression pathways in male mice during EAE were mitochondrial dysfunction and oxidative phosphorylation. Mitochondrial morphology showed significant abnormalities in the cerebral cortex of EAE males, but not EAE females. Regarding function, synaptosomes isolated from cerebral cortex of male EAE mice demonstrated decreased oxygen consumption rates during respirometry assays. Together, cortical neuronal transcriptomics, mitochondrial morphology, and functional respirometry assays in synaptosomes revealed worse neurodegeneration in male EAE mice. This is consistent with worse neurodegeneration in MS men and reveals a model and a target to develop treatments to prevent cortical neurodegeneration and mitigate disability progression in MS men.
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Project description:We sought to more precisely characterize the different alpha-synuclein (aSyn) 3M-bM-^@M-^YUTR mRNA species in normal and PD human brain. High-throughput, whole-transcriptome sequencing of the 3M-bM-^@M-^YUTR ends of polyadenylated mRNA transcripts (termed pA-RNAseq; see Methods) was performed on a cohort of 17 unaffected and 17 PD cerebral cortical tissue samples. This revealed 5 aSyn 3M-bM-^@M-^YUTR isoforms, with lengths of 290, 480, 560, 1070 and 2520 nt. Of these, the 560 nt and 2520 nt forms were predominant. The existence and relative preponderance of these species was further confirmed by Northern Blot. We next hypothesized, that aSyn 3M-bM-^@M-^YUTR selection might be altered in PD. Comparison of pA-RNAseq profiles from PD and unaffected cerebral cortex samples revealed an increase in the preponderance of the long 3M-bM-^@M-^YUTR species (>560 nt) relative to shorter species (<560 nt). Such a relative increase in aSynL was confirmed by Quantitative real-time RT-PCR (rt-qPCR) and appeared specific for PD, as the increase was also observed by comparison to RNA from amyotrophic lateral sclerosis patient samples. We note that the modified aSyn 3M-bM-^@M-^YUTR selection associated with PD patient tissue was detected in cerebral cortex tissue, which typically harbors pathological evidence of the disease process without frank cell loss; thus, this phenotype is unlikely to be a secondary consequence of neurodegeneration. Comparison of 3'UTR ends of alpha-synuclein in PD and unaffected brain cortex
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