GEO DataSets

Analysis of 2 iPSC clones with presenilin 2 (PS2) mutation N141, established by retroviral transduction of fibroblasts from a Familial Alzheimer’s disease (FAD) patient. PS2 mutations are causative factors for autosomal-dominant early-onset FAD. Results provide insight into molecular basis of FAD.

Organism:

Homo sapiens

Type:

Expression profiling by array, count, 3 cell line sets

Platform:

GPL570

Series:

GSE28379

4 Samples

Download data: CEL, CHP

(Submitter supplied) We established two clones of induced pluripotent stem cells (iPSC) with the presenilin 2 mutation, N141 (PS2-1 iPSC and PS2-2 iPSC) by retroviral transduction of primary human fibroblasts. To detect the copy number dependent gene expression profiles in primary fibroblast carrying the presenilin 2 mutation N141(before reprogramming) and PS2-1 iPSC and PS2-2 iPSC(after reprogramming), this experiment was designed.

Organism:

Homo sapiens

Type:

Genome variation profiling by genome tiling array

Platform:

GPL10123

3 Samples

Download data: TXT

(Submitter supplied) We established two clones of induced pluripotent stem cells (iPSC) with the presenilin 2 mutation, N141 (PS2-1 iPSC and PS2-2 iPSC) by retroviral transduction of primary human fibroblasts. To show the similarity among 201B7 iPSC, PD01-25 iPSC(Sporadic Parkinson's disease patient derived iPSC), PS2-1 iPSC, PS2-2 iPSC, this experiment was designed.

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS4141

Platform:

GPL570

4 Samples

Download data: CEL, CHP

(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

(Submitter supplied) Pompe disease is caused by autosomal recessive mutations in the GAA gene, which encodes acid alpha-glucosidase. Although enzyme replacement therapy has recently improved patient survival greatly, the results in skeletal muscles and for advanced disease are still not satisfactory. Here, we report the derivation of Pompe disease induced pluripotent stem cells (PomD-iPSCs) and their potential for pathogenesis modeling, drug testing and disease marker identification. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

12 Samples

Download data: CEL, CHP

(Submitter supplied) Gene expression analysis of control fibroblasts (NFH2), one AD-derived fibroblasts (NFH-46), NFH2-derived control-iPS cells (OiPS3, OiPS6), NFH46-derived AD-iPS cells (iPS5 and iPS 26B), hESCs (H1 and H9).

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL6883

13 Samples

Download data: TXT

(Submitter supplied) gene-expression change along with differentiation stage from human iPS cells to astrocytes is unkown. We used microaray to investigate gene-expression change along with differentiation stage from human iPS cells to astrocytes, and to confirm similarity between human primary astrocyte and iPSC-derived astrocytes.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL6244

7 Samples

Download data: CEL

(Submitter supplied) We generated 10 human iPS-cell clones. We used microarray to evaluate global gene expression pattern, comparing with human ES cell and fibroblast

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL14550

12 Samples

Download data: TXT

(Submitter supplied) Oligomeric forms of amyloid-beta peptide (Abeta) are presumed to play a pivotal role in the pathogenesis of Alzheimer’s disease (AD). However, it is still unclear how Abeta oligomers contribute to AD pathogenesis in patient neural cells. We generated induced pluripotent stem cells (iPSCs) from a familial AD patient and differentiated them into neural cells. Abeta oligomers were accumulated in neural cells of AD bearing amyloid precursor protein (APP)-E693delta mutation. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL6244

6 Samples

Download data: CEL

(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

(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

(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

(Submitter supplied) Non-familial Alzheimer’s disease (AD) occurring before 65 years of age is commonly referred to as early-onset Alzheimer’s disease (EOAD) and constitutes ~5-6% of all Alzheimer’s disease (AD) cases. While EOAD exhibits the same clinicopathological changes such as amyloid plaques, neurofibrillary tangles (NFTs), brain atrophy, and cognitive decline as observed in the more prevalent late-onset AD (LOAD), EOAD patients tend to have more severe cognitive deficits, including visuospatial, language, and motor dysfunction. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24676

24 Samples

Download data: CSV

(Submitter supplied) Late-onset Alzheimer’s disease (LOAD) is the most common form of AD. However, modeling sporadic LOAD, without clear genetic predispositions, to capture hallmark neuronal pathologies such as extracellular amyloid-β (Aβ) plaque deposition, intracellular tau tangles, and neuronal loss, remains an unmet need. Here, we demonstrate that neurons generated by microRNA-based direct reprogramming of fibroblasts from patients affected by autosomal dominant AD (ADAD) and LOAD in a three-dimensional (3D) environment, effectively recapitulate key neuropathological features of AD without additional cellular or genetic insults. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24676

24 Samples

Download data: TXT

(Submitter supplied) Late-onset Alzheimer’s disease (LOAD) is the most common form of AD. However, modeling sporadic LOAD, without clear genetic predispositions, to capture hallmark neuronal pathologies such as extracellular amyloid-β (Aβ) plaque deposition, intracellular tau tangles, and neuronal loss, remains an unmet need. Here, we demonstrate that neurons generated by microRNA-based direct reprogramming of fibroblasts from patients affected by autosomal dominant AD (ADAD) and LOAD in a three-dimensional (3D) environment, effectively recapitulate key neuropathological features of AD without additional cellular or genetic insults. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24676

22 Samples

Download data: TSV

(Submitter supplied) Late-onset Alzheimer’s disease (LOAD) is the most common form of AD. However, modeling sporadic LOAD, without clear genetic predispositions, to capture hallmark neuronal pathologies such as extracellular amyloid-β (Aβ) plaque deposition, intracellular tau tangles, and neuronal loss, remains an unmet need. Here, we demonstrate that neurons generated by microRNA-based direct reprogramming of fibroblasts from patients affected by autosomal dominant AD (ADAD) and LOAD in a three-dimensional (3D) environment, effectively recapitulate key neuropathological features of AD without additional cellular or genetic insults. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24676

48 Samples

Download data: TXT

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Expression profiling by array; Expression profiling by high throughput sequencing

Platforms:

GPL25371 GPL16791

37 Samples

Download data: CEL

(Submitter supplied) Alzheimer’s disease (AD) is preceded by a long prodromal period of decades during which pathology accumulates in the brain prior to the onset of dementia. The molecular basis of these changes as well as how and when they start are unclear. Here we have analyzed neural progenitor (NP) cells and neurons generated from induced pluripotent stem cells (iPSCs) from individuals with sporadic AD (AD) and age-matched controls. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL16791

6 Samples

Download data: TSV

(Submitter supplied) Alzheimer’s disease (AD) is preceded by a long prodromal period of decades during which pathology accumulates in the brain prior to the onset of dementia. The molecular basis of these changes as well as how and when they start are unclear. Here we have analyzed neural progenitor (NP) cells and neurons generated from induced pluripotent stem cells (iPSCs) from individuals with sporadic AD (AD) and age-matched controls. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL25371

10 Samples

Download data: CEL

(Submitter supplied) Alzheimer’s disease (AD) is preceded by a long prodromal period of decades during which pathology accumulates in the brain prior to the onset of dementia. The molecular basis of these changes as well as how and when they start are unclear. Here we have analyzed neural progenitor (NP) cells and neurons generated from induced pluripotent stem cells (iPSCs) from individuals with sporadic AD (AD) and age-matched controls. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL25371

11 Samples

Download data: CEL