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Differential expression analyses in endothelial cells from APP/Psen1 mouse model

ABSTRACT: Differential expression analyses in endothelial cells from APP/Psen1 mouse model

PROVIDER: PRJNA498274 | ENA |

REPOSITORIES: ENA

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Differential expression analyses in endothelial cells from APP/Psen1 mouse model

Project description:Endothelial cells were isolated by flow cytometry using a specific marker (CD31) and their global gene expression profile was analyzed. CD11b marker was contraselected. This data were used to study molecular mechanisms implicated in endothelial cells from App/Psen1 mouse model. In this dataset, we include the expression data obtained in endothelial cells from APP/Psen1 (18 month-old) mouse model using a specific marker for this cell type (CD31+). Functional enrichment analyses were carried out through GSEA, where we have included specific categories potentially involved with blood vessel formation.

2021-03-22 | GSE121729 | GEO

Differential expression analyses in microglial cells from APP-Psen1/+;Cx3cr1-Cre::ERT2/+; Vhl Flox/– mice treated with tamoxifen vs APP-Psen1/+;Cx3cr1-Cre::ERT2/+; Vhl Flox/– mice non treated

Project description:Microglial cells were isolated by flow citometry using specific markers (CD45+/ CD11b+) and their global gene expression profile was analyzed. This data were used to study the role of HIF1A in microglia associated to Aβ plaques. In this dataset, we include the expression data obtained in microglial cells from a model of gain of function of HIF1A in APP-PSEN1/+ mice. (18 moth-old-age) mice model using a specific marker for this cell type (CD31+). Functional enrichment analyses were carried out through GSEA, where we have included specific categories potentially involved with blood vessel formation.

2021-03-08 | GSE168059 | GEO

DNA methylation profiles across different brain regions in APP/PSEN1 mice

Project description:Genome wide DNA methylation profiling of normal and APP/PSEN1 mice. A custom Illumina Golden Gate DNA methylation Beadchip was used to obtain DNA methylation profiles across approximately 800 CpGs. Bisulphite converted DNA from the 96 samples were hybridised to the Illumina custom golden gate DNA methylation array.

2015-12-05 | E-GEOD-42745 | biostudies-arrayexpress

Differential expression analyses in microglial cells from APP-Psen1/+ Cx3cr1-Cre::ERT2/+ Vhl Flox/– mice treated with tamoxifen vs APP-Psen1/+ Cx3cr1-Cre::ERT2/+ Vhl Flox/– mice non treated

Project description:Differential expression analyses in microglial cells from APP-Psen1/+ Cx3cr1-Cre::ERT2/+ Vhl Flox/– mice treated with tamoxifen vs APP-Psen1/+ Cx3cr1-Cre::ERT2/+ Vhl Flox/– mice non treated

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DNA methylation profiles across different brain regions in APP/PSEN1 mice

2015-12-05 | GSE42745 | GEO

Staging Alzheimer’s disease in brains and retinas of APP/PSEN1 mice by transcriptional profiling

Project description:Alzheimer’s disease (AD) is a common form of dementia characterized by amyloid plaque deposition, TAU pathology, neuroinflammation and neurodegeneration. Mouse models recapitulate some key features of AD. For instance, the B6.APP/PS1 model (carrying human transgenes for mutant forms of APP and PSEN1) shows plaque deposition and associated neuroinflammatory responses involving both astrocytes and microglia beginning around 6 months of age. However, in our colony, TAU pathology, significant neurodegeneration and cognitive decline are not apparent in this model even at older ages. Therefore, this model is ideal for studying neuroinflammatory responses to amyloid deposition. Here, RNA sequencing of brain and retinal tissue, generalized linear modeling (GLM), functional annotation followed by validation by immunofluorescence (IF) was performed in B6.APP/PS1 mice to determine the earliest molecular changes prior to and around the onset of plaque deposition (2-6 months of age).

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Transcriptomic and chromatin profiling of familial Alzheimer’s disease mutations in PSEN1, PSEN2, APP [RNA-seq]

Project description:Mutations in PSEN1, PSEN2, and APP cause familial Alzheimer’s Disease (FAD) with an early age at onset and progressive cognitive decline. We mechanistically characterize mutations in these three FAD genes using patient-derived neurons by integrating RNA- and ATAC-sequencing. Here, we demonstrate that FAD mutations share common disease endotypes with varying severity, particularly activation of non-ectoderm lineage and loss of neuron mitochondrial energy production, paving the way for potential therapeutic interventions.

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Transcriptomic and chromatin profiling of familial Alzheimer’s disease mutations in PSEN1, PSEN2, APP [ATAC-seq]

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APP and its intracellular domain modulate Alzheimer’s disease risk gene networks in transgenic APPsw and PSEN1M146I porcine models [hippocampus]

Project description:Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the most frequent cause of dementia. The disease has a substantial genetic component comprising both highly penetrant familial mutations (APP, PSEN1 and PSEN2) and sporadic cases with complex genetic etiology. Mutations in APP and PSEN1/2 alter the proteolytic processing of APP to its metabolites, including Ab and APP Intracellular Domain (AICD). In this study, we use transgenic porcine models carrying the human APPsw and PSEN1M146I transgenes to demonstrate the pathobiological relevance of transcriptional regulation facilitated by APP and its AICD domain. Through molecular characterization of hippocampal tissue, we describe the differential expression of gene sets that cluster in molecular pathways with translational relevance to AD. We further identify phosphorylated and unphosphorylated AICD in differential complexes with proteins implicated in signal transduction and transcriptional regulation. Integrative genomic analysis of transcriptional changes in somatic cell cultures derived from pigs treated with g-secretase inhibitor demonstrates the importance of g-secretase APP processing in transcriptional regulation. Collectively, our data supports a model in which APP, and in particular its AICD domain, modulates gene networks associated with AD pathobiology through interaction with signaling proteins.

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APP and its intracellular domain modulate Alzheimer’s disease risk gene networks in transgenic APPsw and PSEN1M146I porcine models [fibroblasts]

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