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0033de4d-4c32-42e8-ab15-cf0ec3f7009b - samples

ABSTRACT: RNA-sequencing dataset of post-mortem human brain tissue of FTD patients with mutations in GRN, MAPT and C9orf72 and healthy controls.

PROVIDER: EGAD00001008014 | EGA |

REPOSITORIES: EGA

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RNA-seq of human post-mortem brain tissue of the frontal lobe from patients with FTD and healthy controls

Project description:Understanding the molecular mechanisms underlying frontotemporal dementia (FTD) is essential for the development of successful therapies. Systematic studies on human post-mortem brain tissue of patients with genetic subtypes of FTD are currently lacking. The Risk and Modyfing Factors of Frontotemporal Dementia (RiMod-FTD) consortium therefore has generated multi-omics datasets for genetic subtypes of FTD to identify common and distinct molecular mechanisms disturbed in disease. This experiment contains data from RNA-sequencing of human post-mortem brain tissue of the frontal lobe from patients with FTD caused by mutations in GRN, MAPT or C9orf72 and healthy controls.

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CAGE-seq of human post-mortem brain tissue of the frontal lobe from patients with FTD and healthy controls

Project description:Understanding the molecular mechanisms underlying frontotemporal dementia (FTD) is essential for the development of successful therapies. Systematic studies on human post-mortem brain tissue of patients with genetic subtypes of FTD are currently lacking. The Risk and Modyfing Factors of Frontotemporal Dementia (RiMod-FTD) consortium therefore has generated multi-omics datasets for genetic subtypes of FTD to identify common and distinct molecular mechanisms disturbed in disease. This experiment contains data from CAGE-sequencing of human post-mortem brain tissue of the frontal lobe from patients with FTD caused by mutations in GRN, MAPT or C9orf72 and healthy controls.

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smRNA-sequencing of human post-mortem brain tissue of the frontal lobe from patients with Frontotemporal Dementia and healthy controls

Project description:Understanding the molecular mechanisms underlying frontotemporal dementia (FTD) is essential for the development of successful therapies. Systematic studies on human post-mortem brain tissue of patients with genetic subtypes of FTD are currently lacking. The Risk and Modyfing Factors of Frontotemporal Dementia (RiMod-FTD) consortium therefore has generated multi-omics datasets for genetic subtypes of FTD to identify common and distinct molecular mechanisms disturbed in disease. This experiment contains data from smRNA-sequencing of human post-mortem brain tissue of the frontal lobe from patients with FTD caused by mutations in GRN, MAPT or C9orf72 and healthy controls.

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13b2d7b5-4e10-4305-b70e-9459b50c95a4 - samples

Project description:CAGE-sequencing was performed on frontal post-mortem human brain tissue of patients with FTD caused by mutations in GRN, MAPT or C9orf72 and healthy controls.

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Methylation state of human post-mortem brain tissue from the frontal lobe of patients with Frontotemporal Dementia and healthy controls

Project description:Methylation state of human post-mortem brain tissue from the frontal lobe of patients with Frontotemporal Dementia caused by mutations in GRN, MAPT and C9orf72 and healthy controls

2023-02-01 | E-MTAB-12674 | biostudies-arrayexpress

Identification of novel CSF biomarkers in GRN-associated frontotemporal dementia by proteomics

Project description:Frontotemporal dementia is the second most common form of presenile dementia and autosomal dominant inheritance is present in 20-30% of cases, with mutations in granulin (GRN) as a major cause. The exact pathophysiological mechanism by which GRN mutations lead to neurodegeneration is poorly understood. We aimed to identify novel cerebrospinal fluid (CSF) biomarkers in GRN-associated frontotemporal dementia using shotgun proteomics. We included CSF from presymptomatic and symptomatic GRN mutation carriers and healthy non-carriers (controls). We validated our discovery proteomics results in a large international cohort of GRN-mutation carriers and other forms of genetic FTD (C9orf72- and MAPT-mutation carriers) by parallel reaction monitoring.

2019-04-30 | PXD012178 | Pride

Identification of novel CSF biomarkers in GRN-associated frontotemporal dementia by proteomics

2019-04-29 | PXD012179 | Pride

d27d64ef-103b-4a7e-82e5-7ab15dc8cae5 - samples

Project description:This dataset contains smRNA-seq data from post-mortem human brain tissue of the frontal lobe of patients with FTD and healthy controls. The smRNA-sequencing was done in two parts, this dataset depicts the data generated at the DZNE TÃƒÂ¼bingen.

| EGAD00001006846 | EGA

844e08ee-0074-4dff-a4bc-476d59fef00a - samples

Project description:This dataset contains smRNA-seq data from human post-mortem brain tissue of the frontal lobe of patients with FTD and healthy controls. These samples depict the data generated at the DZNE GÃƒÂ¶ttingen and should be used together with the data generated at the DZNE TÃƒÂ¼bingen.

| EGAD00001006845 | EGA

Distinct cell type-specific protein signatures in GRN and MAPT genetic subtypes of frontotemporal dementia

Project description:INTRODUCTION: Frontotemporal dementia (FTD) is characterized by progressive atrophy of frontal and/or temporal cortices and considerable clinical, pathological, and genetic heterogeneity. METHODS: Frontal and temporal cortex tissues from FTD-GRN (n=9), FTD-MAPT (n=13), and non-demented controls (n=11) were analysed with quantitative proteomics (DIA). Expression-weighted cell type enrichment deduced the role of major brain cell types and gene ontology analysis identified distinct biological processes. FTD-MAPT data was also compared to an AD (n=10) protein signature. RESULTS: We identified brain region-specific FTD protein expression signatures. In frontal cortex of FTD-GRN, we observed immune processes in endothelial cells and mitochondrial dysregulation in neurons. In temporal cortex of FTD-MAPT, we observed dysregulated RNA processing, oligodendrocyte dysfunction, and axonal impairment. Comparison with AD indicated that alterations in RNA processing and oligodendrocyte function are distinct for FTD-MAPT. DISCUSSION: Our results indicate cell type-specific biological processes distinctive for genetic FTD subtypes. These findings may aid the development of FTD subtype-specific treatment strategies.

2022-08-12 | PXD031419 | Pride

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