Genotyping data from subjects with brain lesions
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PROVIDER: PRJNA1170351 | ENA |
REPOSITORIES: ENA
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Project description:Genotyping data from subjects with brain lesions
| PRJNA1170352 | ENA
Project description:Data from the VLA lyssavirus genotyping microarray. The array platform for this data is GEO accession GPL8066, and consists of 624 oligos representing two viral families. The data set itself consists of 14 arrays, 7 hybridised with RNA from mice brains infected with 7 genotypes of lyssaviruses, 1 hybridised with RNA from normal mouse brain, and 6 hybridised with RNA from coded samples consisting of infected mouse brains or control mouse brains. Keywords: Lyssavirus genotyping microarray
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Project description:Genome wide DNA methylation profiles of various human brain regions (cerebellum, occipital lobe, etc). The Illumina Infinium 450k Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation profiles across approximately 480,000 CpGs. The dataset includes 130 samples. Multiple brain regions were assessed per subject. The goal was to evaluate the effect of HIV infection on DNA methylation levels. Genome wide DNA methylation profiles of various brain regions from HIV positive and negative subjects. The Illumina Infinium 450k Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation profiles across approximately 480,000 CpGs. Dataset included 130 samples: 99 samples from HIV+ subjects and 31 samples from HIV- subjects. The Illumina Infinium450 platform was applied to various brain regions from HIV+ and HIV- subjects. We evaluated 130 brain samples from 84 different subjects. Specifically, we considered cerebellum (20 HIV+ samples and 4 controls), frontal lobe (2 cases, 4 controls), hippocampus (4 controls), medial frontal cortex (18 cases), occipital cortex (59 cases, 13 controls), temporal cortex (4 controls). In total, there were 99 samples from HIV+ subjects and 31 samples from HIV- controls of similar ages. The subjects were recruited from the National Neurological AIDS Bank study or Multicenter AIDS Cohort study in Los Angeles. Informed consent and all study procedures were approved by the UCLA Medical IRB. DNAm data from HIV+ cases and HIV- controls were generated at the same time and randomized across plates and chips. HIV viral load information was available for blood (measured at the last blood draw) and for cerebrospinal fluid (CSF).
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Project description:Human DNA methylation Beadchip v1.2 was used to profile n=475 samples from various brain regions of subjects with Huntington's disease and control samples. The main goal of the study was to relate Huntington's disease status to measures of epigenetic age acceleration based on DNA methylation data. To measure DNA methylation age, we used the epigenetic clock software described in Horvath S (n=2013) DNA methylation age of human tissues and cell types. Genome Biology.2013, 14:R115. DOI: 10.1186/10.1186/gb-2013-14-10-r115 PMID: 24138928.
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Project description:Genome wide DNA methylation profiles of various human brain regions (cerebellum, occipital lobe, etc). The Illumina Infinium 450k Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation profiles across approximately 480,000 CpGs. The dataset includes 130 samples. Multiple brain regions were assessed per subject. The goal was to evaluate the effect of HIV infection on DNA methylation levels. Genome wide DNA methylation profiles of various brain regions from HIV positive and negative subjects. The Illumina Infinium 450k Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation profiles across approximately 480,000 CpGs. Dataset included 130 samples: 99 samples from HIV+ subjects and 31 samples from HIV- subjects.
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Project description:Here, we investigated whether cuprizone-induced oligodendrocyte apoptosis is sufficient to trigger peripheral immune cell recruitment into the forebrain. We show that early cuprizone-induced white matter lesions display a striking similarity to early MS lesions, i.e., oligodendrocyte degeneration, microglia activation and absence of lymphocytes. Such early cuprizone lesions are sufficient to trigger peripheral immune cell recruitment. The lesions are characterized by discontinuation of the perivascular glia limitans, focal axonal damage, and perivascular astrocyte pathology. Time course studies showed that the severity of cuprizone-induced lesions positively correlates with the extent of peripheral immune cell recruitment. Furthermore, results of genome-wide array analyses suggest that moesin is integral for early microglia activation in cuprizone and MS lesions. This study underpins the significance of brain-intrinsic degenerative cascades for immune cell recruitment and, in consequence, MS lesion formation.
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