Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Osteopontin drives neuroinflammation and cell loss in MAPT-N279K frontotemporal dementia patient neurons

ABSTRACT: Osteopontin drives neuroinflammation and cell loss in MAPT-N279K frontotemporal dementia patient neurons

PROVIDER: PRJNA961689 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR24299732_1.fastq.gz	Fastqsanger.gz
	SRR24299732_2.fastq.gz	Fastqsanger.gz
	SRR24299733_1.fastq.gz	Fastqsanger.gz
	SRR24299733_2.fastq.gz	Fastqsanger.gz
	SRR24299734_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 90

Similar Datasets

Osteopontin drives neuroinflammation and cell loss in MAPT-N279K frontotemporal dementia patient neurons

Project description:Frontotemporal dementia (FTD) is an incurable group of early-onset dementias that can be caused by deposition of hyperphosphorylated tau in patient brains. However, the mechanisms leading to neurodegeneration remain largely unknown. Here, we combined single-cell analyses of FTD patient brains with a stem cell culture and transplantation model of FTD. We identified disease phenotypes in FTD neurons carrying the MAPT-N279K mutation, which were related to oxidative stress, oxidative phosphorylation and neuroinflammation with an upregulation of the inflammation-associated protein osteopontin (OPN). Human FTD neurons survived less and elicited an increased microglial response after transplantation into the mouse forebrain, that we further characterized by single nucleus RNA-sequencing of microdissected grafts. Notably, downregulation of OPN in engrafted FTD neurons resulted in improved engraftment and reduced microglial infiltration, indicating an immune-modulatory role of OPN in patient neurons, which may represent a potential therapeutic target in FTD.

2024-04-15 | GSE230519 | GEO

Osteopontin drives neuroinflammation and cell loss in MAPT-N279K frontotemporal dementia patient neurons

2024-04-15 | GSE230450 | GEO

Osteopontin drives neuroinflammation and cell loss in MAPT-N279K frontotemporal dementia patient neurons

2024-04-15 | GSE230447 | GEO

Osteopontin drives neuroinflammation and cell loss in MAPT-N279K frontotemporal dementia patient neurons

Project description:Osteopontin drives neuroinflammation and cell loss in MAPT-N279K frontotemporal dementia patient neurons

| PRJNA961691 | ENA

Osteopontin drives neuroinflammation and cell loss in MAPT-N279K frontotemporal dementia patient neurons

Project description:Osteopontin drives neuroinflammation and cell loss in MAPT-N279K frontotemporal dementia patient neurons

| PRJNA961152 | ENA

Osteopontin drives neuroinflammation and cell loss in MAPT-N279K frontotemporal dementia patient neurons

Project description:Osteopontin drives neuroinflammation and cell loss in MAPT-N279K frontotemporal dementia patient neurons

| PRJNA961142 | ENA

A role for astrocytic miR-129-5p in Frontotemporal Dementia

Project description:Frontotemporal dementia is a debilitating neurodegenerative disorder characterized by frontal and temporal lobe degeneration, resulting in behavioral changes, language difficulties, and cognitive decline. In this study, smallRNA sequencing was conducted on postmortem brain tissues obtained from FTD patients with GRN, MAPT, or C9ORF mutations, focusing on the frontal and temporal lobes. Our analysis identified miR-129-5p as consistently deregulated across all mutation conditions and brain regions. Functional investigations revealed a novel role of miR-129-5p in astrocytes, where its loss led to neuroinflammation and impaired neuronal support functions, including glutamate uptake. Depletion of miR-129-5p in astrocytes resulted in the loss of neuronal spines and altered neuronal network activity. These findings highlight miR-129-5p as a potential therapeutic target in neurodegenerative diseases and also sheds light on the role of astrocytes in Frontotemporal dementia pathogenesis.

2025-04-17 | GSE262895 | GEO

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

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.

2023-02-26 | E-MTAB-12731 | biostudies-arrayexpress

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data