Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Inflammasome signaling is dispensable for ß-amyloid-induced neuropathology in preclinical models of Alzheimer's disease

ABSTRACT: Inflammasome signaling is dispensable for ß-amyloid-induced neuropathology in preclinical models of Alzheimer's disease

PROVIDER: PRJNA1049814 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR27130079_1.fastq.gz	Fastqsanger.gz
	SRR27130079_2.fastq.gz	Fastqsanger.gz
	SRR27130080_1.fastq.gz	Fastqsanger.gz
	SRR27130080_2.fastq.gz	Fastqsanger.gz
	SRR27130081_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 20

Similar Datasets

Inflammasome signaling is dispensable for ß-amyloid-induced neuropathology in preclinical models of Alzheimer's disease

Project description:Alzheimer's disease (AD) is the most common neurodegenerative disorder affecting memory and cognition. The disease is accompanied by an abnormal deposition of ß-amyloid plaques in the brain that contributes to neurodegeneration and is known to induce glial inflammation. Studies in the APP/PS1 mouse model of ß-amyloid-induced neuropathology have suggested a role for inflammasome activation in ß-amyloid-induced neuroinflammation and neuropathology. Here, we evaluated the in vivo role of microglia-selective and full body inflammasome signalling in several mouse models of ß-amyloid-induced AD neuropathology. Unexpectedly, microglia-specific deletion of the inflammasome regulator A20 and inflammasome effector protease caspase-1 in the AppNL-G-F and APP/PS1 models failed to identify a prominent role for microglial inflammasome signalling in ß-amyloid-induced neuropathology. Moreover, global inflammasome inactivation through respectively full body deletion of caspases 1 and 11 in AppNL-G-F mice and Nlrp3 deletion in APP/PS1 mice, also failed to modulate amyloid pathology and disease progression. In agreement, single-cell RNA sequencing did not reveal an important role for Nlrp3 signalling in driving microglial activation and the transition into disease-associated states, both during homeostasis and upon amyloid pathology. Collectively, these results question a generalizable role for inflammasome activation in pre-clinical amyloid-only models of neuroinflammation.

2024-01-17 | GSE249611 | GEO

Inflammasome signaling is dispensable for ß-amyloid-induced neuropathology in preclinical models of Alzheimer's disease.

Project description: Not available

| S-EPMC10863058 | biostudies-literature

Comparative analysis of transcriptome remodeling in plaque associated and plaque distant microglia during amyloid-ß pathology progression

Project description:In this study, we combined cell-specific laser capture and RNA-seq analysis to investigate transcriptome changes in both amyloid-ß plaque-associated and plaque-distant microglia at different stages of the disease.

2022-09-28 | GSE205048 | GEO

Methylomic signatures of tau and beta amyloid in transgenic mouse models of Alzheimer’s disease neuropathology [RRBS]

Project description:We identified widespread DNA methylation changes associated with the development of both tau and amyloid neuropathology, including differentially methylated positions (DMPs) and regions (DMRs) at loci previously implicated in AD and overlapping changes identified in our ongoing analyses of human post-mortem AD brains.

2024-10-30 | GSE246560 | GEO

Methylomic signatures of tau and beta amyloid in transgenic mouse models of Alzheimer’s disease neuropathology [HorvathMammalMethylChip40 Methylation Beadchip]

2024-10-30 | GSE246559 | GEO

Synergistic behavioral and neuroinflammatory effects of amyloid neuropathology and sepsis survival in a murine model of Alzheimer’s disease II

Project description:Synergistic behavioral and neuroinflammatory effects of amyloid neuropathology and sepsis survival in a murine model of Alzheimer’s disease. 72 post-mortem perfused brain tissue samples from male and female mice (5xFAD and C57BL/6) with and without sepsis, 25 days post CLP infection.

2025-06-04 | GSE176505 | GEO

Synergistic behavioral and neuroinflammatory effects of amyloid neuropathology and sepsis survival in a murine model of Alzheimer’s disease I

Project description:Synergistic behavioral and neuroinflammatory effects of amyloid neuropathology and sepsis survival in a murine model of Alzheimer’s disease. 40 post-mortem perfused brain tissue samples from both male and female mice (5xFAD and C57BL/6) with and without sepsis, 5 days post CLP infection.

2025-06-04 | GSE176504 | GEO

Transcriptional signatures of progressive neuropathology in tau and amyloid mouse models

Project description:Transcriptional signatures of progressive neuropathology in tau and amyloid mouse models

| PRJNA518104 | ENA

The ATP-P2X7 signaling axis is dispensable for obesity-associated inflammasome activation in adipose tissue

Project description:Inflammasome activation in adipose tissue has been implicated in obesity-associated insulin resistance and type 2 diabetes. However, when and how inflammasome is activated in adipose tissue remains speculative. Here we test the hypothesis that extracellular ATP, a potent stimulus of inflammasome in macrophages via purinergic receptor P2X, ligand-gated ion channel, 7 (P2X7), may play a role in inflammasome activation in adipose tissue in obesity. Our data show that inflammasome is activated in adipose tissue upon 8-week feeding of 60% HFD, coinciding with the onset of hyperglycemia and hyperinsulinemia as well as the induction of P2X7 in adipose tissue. Unexpectedly, P2X7-deficient animals on HFD exhibit no changes in metabolic phenotypes, nor in inflammatory responses or inflammasome activation when compared to the wildtype controls. Similar observations have been obtained in hematopoietic cell-specific P2X7-deficient animals generated by bone marrow transplantation. Thus, we conclude that inflammasome activation in adipose tissue in obesity coincides with the onset of hyperglycemia and hyperinsulinemia, but unexpectedly, is not mediated by the ATP-P2X7 signaling axis. The nature of the inflammasome-activating danger signal(s) in adipose tissue in obesity remains to be characterized. Wild type and P2X7 knockout mice were fed a low fat diet (chow) or high fat diet for 12 weeks. After the diet intervention period, the animals were killed and epididymal white adipose tissue was removed. Total RNA was isolated and subjected to gene expression profiling.

2012-02-24 | E-GEOD-36033 | biostudies-arrayexpress

Expression profiling of laser-microdissected tissue from APPPS1 plaque-depositing mouse model of Alzheimer's disease

Project description:Amyloid-ß (Aß) plaques are pathological hallmarks of Alzheimer disease. However, the precise neuropathological changes that occur in brain in response to amyloid deposition are largely unknown. To study the molecular mechanism(s) responsible for Aß-mediated neuropathology, we performed a gene expression analysis on frontal neocortical brain tissue of APPPS1 mice compared to their littermate controls.

2014-11-04 | GSE15058 | GEO

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