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Links from GEO DataSets

Items: 20

1.

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]

(Submitter supplied) 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
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
12 Samples
Download data: TXT
Series
Accession:
GSE128344
ID:
200128344
2.

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

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
24 Samples
Download data
Series
Accession:
GSE128345
ID:
200128345
3.

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]

(Submitter supplied) 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
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
12 Samples
Download data: TXT
Series
Accession:
GSE128343
ID:
200128343
4.

Probing sporadic and familial Alzheimer?s disease using induced pluripotent stem cells.

(Submitter supplied) Our understanding of Alzheimer’s disease (AD) pathogenesis is currently limited by difficulties in obtaining live neurons from patients and the inability to model the sporadic form of AD. It may be possible to overcome these challenges by reprogramming primary cells from patients into induced pluripotent stem cells (iPSCs). We reprogrammed primary fibroblasts from two patients with familial AD (both caused by a duplication of APP1, APPDp), two with sporadic AD (sAD1, 2) and two non-demented control individuals (NDCs) into iPSC lines. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
38 Samples
Download data: TXT
Series
Accession:
GSE34879
ID:
200034879
5.

The transcriptomic landscape of glutamatergic cortical neurons carrying Alzheimer’s disease PSEN1 mutations reveals alterations in structural components, signalling, and ncRNA regulation

(Submitter supplied) To investigate gene expression changes related to two fAD mutations (A79V and L150P) in the Presenilin-1 gene (PSEN1) we compared the transcriptomes (polyA and total) of glutamatergic cortical neurons derived from fAD-mutant human induced pluripotent stem cells and their individual isogenic controls generated via precision CRISPR/Cas9 genome editing.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL28038
40 Samples
Download data: GTF, TSV
Series
Accession:
GSE211993
ID:
200211993
6.

APP levels mediate beta-amyloid but not tau-related aspects of Alzheimer’s disease in a Down syndrome model of cortical neurogenesis.

(Submitter supplied) Early-onset Alzheimer’s disease-like pathology in Down syndrome (DS, trisomy 21) is commonly attributed to an increased dosage of the amyloid precursor protein (APP) gene. To test this central tenet of the amyloid-cascade hypothesis we deleted the supernumerary copy of the APP gene in trisomic DS iPSC, or upregulated APP expression in euploid human pluripotent stem cell lines with dCas9-VP64, and subjected these lines to prolonged cortical neural differentiation. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
34 Samples
Download data: TXT
Series
Accession:
GSE100680
ID:
200100680
7.

Xenografted human iPSC-derived neurons with the familial Alzheimer’s disease APPV717I mutation reveal dysregulated transcriptome signatures linked to synaptic function and implicate LINGO2 as a disease signaling mediator

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below. Alzheimer’s disease (AD) is the most common cause of dementia, and disease mechanisms are still not fully understood. Here, we explored pathological changes in human induced pluripotent stem cell (iPSC)-derived neurons carrying the familial AD APPV717I mutation after cell injection into the mouse forebrain. APPV717I mutant iPSCs and isogenic controls were differentiated into neurons revealing enhanced Aβ42 production, elevated phospho-tau, and impaired neurite outgrowth in APPV717I neurons. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
30 Samples
Download data
Series
Accession:
GSE231640
ID:
200231640
8.

Xenografted human iPSC-derived neurons with the familial Alzheimer’s disease APPV717I mutation reveal dysregulated transcriptome signatures linked to synaptic function and implicate LINGO2 as a disease signaling mediator

(Submitter supplied) Alzheimer’s disease (AD) is the most common cause of dementia, and disease mechanisms are still not fully understood. Here, we explored pathological changes in human induced pluripotent stem cell (iPSC)-derived neurons carrying the familial AD APPV717I mutation after cell injection into the mouse forebrain. APPV717I mutant iPSCs and isogenic controls were differentiated into neurons revealing enhanced Aβ42 production, elevated phospho-tau, and impaired neurite outgrowth in APPV717I neurons. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
18 Samples
Download data: CSV
Series
Accession:
GSE231639
ID:
200231639
9.

Xenografted human iPSC-derived neurons with the familial Alzheimer’s disease APPV717I mutation reveal dysregulated transcriptome signatures linked to synaptic function and implicate LINGO2 as a disease signaling mediator

(Submitter supplied) Alzheimer’s disease (AD) is the most common cause of dementia, and disease mechanisms are still not fully understood. Here, we explored pathological changes in human induced pluripotent stem cell (iPSC)-derived neurons carrying the familial AD APPV717I mutation after cell injection into the mouse forebrain. APPV717I mutant iPSCs and isogenic controls were differentiated into neurons revealing enhanced Aβ42 production, elevated phospho-tau, and impaired neurite outgrowth in APPV717I neurons. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
12 Samples
Download data: CSV
Series
Accession:
GSE231638
ID:
200231638
10.

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

(Submitter supplied) 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. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
14 Samples
Download data: TXT
11.

APOE4 Causes Widespread Molecular and Cellular Alterations Associated with Alzheimer's Disease Phenotypes in Human iPSC-Derived Brain Cell Types

(Submitter supplied) The apolipoprotein E4 (APOE4) variant is the single greatest genetic risk factor for sporadic Alzheimer's disease (sAD). However, the cell-type-specific functions of APOE4 in relation to AD pathology remain understudied. Here, we utilize CRISPR/Cas9 and induced pluripotent stem cells (iPSCs) to examine APOE4 effects on human brain cell types. Transcriptional profiling identified hundreds of differentially expressed genes in each cell type, with the most affected involving synaptic function (neurons), lipid metabolism (astrocytes), and immune response (microglia-like cells). more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL18573 GPL11154
26 Samples
Download data: TXT
12.

Human PSEN1 Mutant Glia Improve Spatial Learning and Memory in Aged Mice

(Submitter supplied) PSEN1 ΔE9 mutation causes a familial form of Alzheimer's disease. We have previously shown that human induced pluripotent stem cell (iPSC)-derived astrocytes carrying PSEN1 ΔE9 mutation exhibit transcriptional and functional abnormalities (Stem Cell Reports. 2017;9:1885-1897). Here we injected glial progenitors derived from 2 pairs of PSEN1 ΔE9 mutant- isogenic CTRL iPSCs intracerebroventricularly into newborn mice. more...
Organism:
Mus musculus; Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19415
11 Samples
Download data: TXT
Series
Accession:
GSE221027
ID:
200221027
13.

Region specific astrocyte response to mutant GFAP in Alexander disease model mice during postnatal development.

(Submitter supplied) Gene expression analysis was performed in Gfap+/+, Gfap+/R236H, and mGFAPTg170-2 transgenic mice, using the Aldh1l1-eGFP-L10a transgenic line (JD130) to isolate translating ribosomes and purify astrocyte specific transcripts for RNAseq.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
18 Samples
Download data: CSV
Series
Accession:
GSE198817
ID:
200198817
14.

Genetic modifiers of GFAP expression in mouse models of Alexander disease

(Submitter supplied) Gene expression analysis was performed in mouse models with Alexander disease associated GFAP mutations
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
16 Samples
Download data: CSV
Series
Accession:
GSE197044
ID:
200197044
15.

Efficient manipulation of gene dosage in human iPSCs using CRISPR/Cas9 nickases

(Submitter supplied) The dysregulation of gene dosage due to duplication or haploinsufficiency is a major cause of autosomal dominant diseases such as Alzheimer’s disease. However, there is no rapid and efficient method for manipulating gene dosage in a human model system such as human induced pluripotent stem cells (iPSCs). Here, we describe a simple and precise method to simultaneously generate iPSC lines with different gene dosages using paired Cas9 nickases. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
9 Samples
Download data: CSV
16.

RNA-binding protein ELAVL4/HuD ameliorates Alzheimer's disease-related molecular changes in human iPSC-derived neurons

(Submitter supplied) We generated ELAVL4 knockout (KO), overexpression (OE), and rescue human induced pluripotent stem cell-derived neurons to study the effect that ELAVL4 has on AD-related cellular phenotypes. To gain insight into the molecular cascades involved in neuronal ELAVL4 signaling, we then performed gene expression profiling analysis using data obtained from RNA-seq using triplicate samples for each condition
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21290
48 Samples
Download data: TSV, XLSX
Series
Accession:
GSE202985
ID:
200202985
17.

Endotype reversal as a novel strategy for screening drugs targeting familial Alzheimer's disease

(Submitter supplied) While amyloid-β (Aβ) plaques are considered a hallmark of Alzheimer's disease, clinical trials focused on targeting gamma secretase, an enzyme involved in aberrant Aβ peptide production, have not led to amelioration of AD symptoms or synaptic dysregulation. Screening strategies based on mechanistic, multi-omics approaches that go beyond pathological readouts can aid in the evaluation of therapeutics. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
11 Samples
Download data: TXT
18.

iPSC-Derived PSEN2 (N141I) astrocytes and microglia exhibit a primed inflammatory phenotype

(Submitter supplied) Background: Widescale evidence points to the involvement of glia and immune pathways in the progression of Alzheimer’s disease (AD). AD-associated iPSC-derived glial cells show a diverse range of AD-related phenotypic states encompassing cytokine/chemokine release, phagocytosis and morphological profiles, but to date studies are limited to cells derived from PSEN1, APOE and APP mutations or sporadic patients. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
7 Samples
Download data: TXT
Series
Accession:
GSE243177
ID:
200243177
19.

Neuronal and glial Gene expression from control and healthy patient iPSC-derived cortical neurons

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
unidentified; Homo sapiens
Type:
Expression profiling by array
Platforms:
GPL21292 GPL21293
104 Samples
Download data: RCC
Series
Accession:
GSE76551
ID:
200076551
20.

Neuronal and glial Gene expression from control and healthy patient iPSC-derived cortical neurons (B)

(Submitter supplied) Neuronal or glial cell fates related gene expression from single cells with variety of sAPPa or total Aβ secretion profiles were presented here.
Organism:
unidentified; Homo sapiens
Type:
Expression profiling by array
Platform:
GPL21292
32 Samples
Download data: RCC
Series
Accession:
GSE76547
ID:
200076547
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