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A large panel of isogenic APP and PSEN1 mutant human iPSC neurons reveals shared endosomal abnormalities mediated by APP b-CTFs, not Ab [RNA-seq]

ABSTRACT: A large panel of isogenic APP and PSEN1 mutant human iPSC neurons reveals shared endosomal abnormalities mediated by APP b-CTFs, not Ab [RNA-seq]

PROVIDER: PRJNA527202 | ENA |

REPOSITORIES: ENA

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A large panel of isogenic APP and PSEN1 mutant human iPSC neurons reveals shared endosomal abnormalities mediated by APP b-CTFs, not Ab

Project description:A large panel of isogenic APP and PSEN1 mutant human iPSC neurons reveals shared endosomal abnormalities mediated by APP b-CTFs, not Ab

| PRJNA527199 | ENA

A large panel of isogenic APP and PSEN1 mutant human iPSC neurons reveals shared endosomal abnormalities mediated by APP b-CTFs, not Ab [ribosome profiling]

Project description:A large panel of isogenic APP and PSEN1 mutant human iPSC neurons reveals shared endosomal abnormalities mediated by APP b-CTFs, not Ab [ribosome profiling]

| PRJNA527204 | ENA

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 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

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

2015-12-05 | GSE42745 | GEO

A large panel of isogenic APP and PSEN1 mutant human iPSC neurons reveals shared endosomal abnormalities mediated by APP b-CTFs, not Ab

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-08-08 | GSE128345 | GEO

A large panel of isogenic APP and PSEN1 mutant human iPSC neurons reveals shared endosomal abnormalities mediated by APP b-CTFs, not Ab [ribosome profiling]

Project description:Human iPS cells with different mutations linked to Alzheimer's Disease were differentiated into neurons and subjected to ribosome profiling to identify Alzheimer's Disease associated changes

2019-08-08 | GSE128344 | GEO

A large panel of isogenic APP and PSEN1 mutant human iPSC neurons reveals shared endosomal abnormalities mediated by APP b-CTFs, not Ab [RNA-seq]

Project description:Human iPS cells with different mutations linked to Alzheimer's Disease were differentiated into neurons and subjected to RNAseq to identify Alzheimer's Disease associated changes

2019-08-08 | GSE128343 | GEO

The Alzheimer’s gene SORL1 is a key regulator of endosomal recycling in human neurons

Project description:Loss of the Sortilin-related receptor 1 (SORL1) gene seems to act as a causal event for Alzheimer’s disease (AD). Recent studies have established that loss of SORL1, as well as mutations in autosomal dominant AD genes APP and PSEN1/2, pathogenically converge by swelling early endosomes, AD’s cytopathological hallmark. Acting together with the retromer trafficking complex, SORL1 has been shown to regulate the recycling of the amyloid precursor protein (APP) out of the endosome, contributing to endosomal swelling and to APP misprocessing. We hypothesized that SORL1 plays a broader role in neuronal endosomal recycling and used human induced pluripotent stem cell derived neurons (hiPSC-Ns) to test this hypothesis. In SORL1 deficient (SORL1KO) cell lines, we map the trafficking of the glutamate receptor and the BDNF neurotrophic receptor, two kinds of transmembrane proteins that depend on endosomal recycling and that are linked to AD pathophysiology. We find that as with APP, SORL1 is required for efficient endosomal recycling of the glutamate receptor AMPA1 (GLUA1) and the BDNF receptor Tropomyosin-related kinase B (TRKB). Next, we used cell lines engineered to overexpress SORL1 and find that increased SORL1 expression enhances recycling for APP and GLUA1. Finally, we performed an unbiased transcriptomic screen of SORL1KO neurons and the data further support SORL1’s role in endosomal recycling. We observed altered expression networks that regulate cell surface trafficking and neurotrophic signaling. Collectively, and together with other recent observations, these findings suggest that SORL1 is a key and broad regulator of retromer-dependent endosomal recycling in neurons, a conclusion that has both pathogenic and therapeutic implications.

2022-03-01 | GSE180793 | 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).

2019-11-25 | GSE136861 | GEO

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