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Ena-DATASET-CBMSO-18-05-2017-11:05:52:569-80 - samples

ABSTRACT: Sequence data from fungal infection isolated from neural tissue in ALS patients.

PROVIDER: EGAD00001003341 | EGA |

REPOSITORIES: EGA

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Fungal infection in neural tissue from Amyotrophic Lateral Sclerosis

Project description:The study shows that fungus infection, isolated from neural tissue, can be a risk factor to develop Amyothophic lateral sclerosis (ALS).

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ena-DATASET-CBMSO-19-12-2017-10:59:25:688-77 - samples

Project description:In the present study, we have examined fungal and bacterial infection in brain tissue from 10 AD patients and 16 control subjects by next-generation sequencing NGS using MiSeq sequencing platform (Illumina).

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ena-DATASET-CBMSO-01-03-2017-14:53:11:536-19 - samples

Project description:Amplicon-based fungal metagenomic sequencing for the identification of fungal species in brain tissue from Alzheimer's disease. The study consists in 14 samples, sequenced using Illumina's paired-end technology.

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Whole genome sequencing reveals that variants in the Interleukin 18 Receptor Accessory Protein 3′UTR protect against ALS

Project description:The non-coding genome is substantially larger than the protein-coding genome, but has been largely unexplored by genetic association studies. Here, we performed region-based rare-variant association analysis of >25,000 variants in untranslated regions of 6,139 amyotrophic lateral sclerosis (ALS) whole-genomes and those of 70,403 non-ALS controls. We identified Interleukin-18 Receptor Accessory Protein (IL18RAP) 3′UTR variants as significantly enriched in non-ALS genomes and associated with five-fold reduced risk of developing ALS, and this was replicated in an independent cohort. These variants in the IL18RAP 3′UTR reduce mRNA stability and the binding of double-stranded RNA-binding proteins. Finally, the variants of IL18RAP 3′UTR confer a survival advantage for motor neurons because they dampen neurotoxicity of human iPSC-derived microglia bearing an ALS-associated expansion in C9orf72, and this depends on NF-κB signaling. This study reveals genetic variants that protect against ALS by reducing neuroinflammation, and emphasizes the importance of non-coding genetic association studies.

2022-02-09 | GSE186757 | GEO

ena-DATASET-CBMSO-16-05-2019-08:09:24:047-226 - samples

Project description:Isolation of fungi in infected neural tissues in patients with Parkinson's disease. Here we used next generation sequencing of Internal Transcribed Spacer (ITS) regions, by PCR amplicons (NGS ITS amplicon analysis).

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ena-DATASET-KNIH-31-07-2017-05:52:51:642-1228 - samples

Project description:A IPS05_X_NPC_smRNA-Seq single end data for Neural progenitor cells(Nestin)

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Large-scale rewiring of innate immunity circuitry and microRNA regulation during initial rice blast infection [smallRNA-Seq]

Project description:Rice blast is a recurrent fungal disease, and resistance to fungal infection is a complex trait. Therefore, a comprehensive examination of rice transcriptome and its variation during fungal infection is necessary to understand the complex gene regulatory networks. In this study, adopting Next-Generation Sequencing we profiled the transcriptomes and microRNAomes of rice varieties, one susceptible and the other resistant to M. oryzae, at multiple time points during the fungal infection.

2016-05-01 | GSE77332 | GEO

Large-scale rewiring of innate immunity circuitry and microRNA regulation during initial rice blast infection [RNA-Seq]

2016-05-01 | GSE77331 | GEO

Labour market position of young people and premature mortality in adult life: A 26-year follow-up of 569 528 Swedish 18 year-olds.

Project description:BackgroundThroughout the industrialized world, demand for low skilled labour is falling. The length of schooling is increasing in response, but so is the proportion of individuals not finishing upper secondary school. The objective of this study was to evaluate the associations between labour market positions at age 18 and all-cause and suicide- and accident-specific mortality in later adulthood.MethodsLabour market positions at age 18 were categorized for all Swedes born 1972-77 (n=630 959) into four main groups: employed, successful students, students not about to qualify (SNAQs), and individuals not in employment, education or training (NEETs). Cox proportional hazard models were fitted to assess all-cause, suicide and accident mortality up to 2016 (ages 39-44), adjusting for high school grades, parental and own prior psychiatric diagnoses, and childhood socioeconomic status.FindingsSNAQs had substantially increased all-cause (men: HR=2.10; 95% CI 1.92-2.28, women: HR=1.64; 95% CI: 1.44-1.86), suicide (men: HR=2.16; CI: 1.86-2.51, women: HR=2.10; 95% CI 1.64-2.69), and accident specific (men: HR=2.08; 95% CI 1.77-2.44, women: 1.87; 95% CI 1.33;2.62) mortality risks compared to successful students. The risks were similar for NEETs. There was no increased risk among full-time employed compared to successful students.InterpretationExpanding the educational system may be a natural response to falling demand for low skilled labour but not by far one that corrects the major societal challenge of it. Unless educational systems adequately respond to this challenge, only more inequality is to be expected ahead.FundingThis work was supported by a grant to FR and AL from the Swedish Research Council for Health, Working Life, and Welfare with contract number (2014-2009).

| S-EPMC8454531 | biostudies-literature

Transcriptomic profiling of purified mature olfactory sensory neurons from transgenic mice expressing genomically encoded double-stranded RNA

Project description:Triggers of innate immune signaling in the CNS of amyotrophic lateral sclerosis and frontotemporal degeneration (ALS/FTD) patients remain elusive. We report the presence of cytoplasmic double-stranded RNA (cdsRNA), an established trigger of innate immunity, in ALS-FTD brains carrying C9ORF72 intronic hexanucleotide expansions that included genomically encoded expansions of the G4C2 repeat sequences. Presence of cdsRNA in human brains was coincident with cytoplasmic TDP-43 inclusions, a pathologic hallmark of ALS/FTD. Introducing cdsRNA into cultured human neural cells induced Type I interferon (IFN-I) signaling and death that was rescued by FDA-approved JAK inhibitors. In mice, genomically encoded dsRNAs expressed exclusively in a neuronal class induced IFN-I and death in connected neurons non-cell autonomously. Our findings establish that genomically encoded cdsRNAs trigger sterile, viral-mimetic IFN-I induction, and propagated death within neural circuits and may drive neuroinflammation and neurodegeneration in ALS/FTD patients.

2021-03-01 | GSE166307 | GEO

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