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Links from GEO DataSets

Items: 20

1.

TREM2 regulates microglial cholesterol metabolism upon chronic phagocytic challenge

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL24247 GPL21103
134 Samples
Download data
Series
Accession:
GSE130627
ID:
200130627
2.

TREM2 regulates microglial lipid metabolism during aging in mice [RNA-Seq]

(Submitter supplied) TREM2 is a microglial-specific gene implicated in late-onset Alzheimer's Disease (AD). Recent studies have identified that Trem2-deficient mice exhibit transcriptional changes in microglial gene expression that minimize the upregulation of lipid metabolism and lysosomal genes in AD disease models. We detect similiarly attenuated expression of lipid metabolism genes in microglia isolated from brains of aged Trem2 knockout mice.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
56 Samples
Download data: TAB
Series
Accession:
GSE134031
ID:
200134031
3.

TREM2 regulates microglial cholesterol metabolism upon chronic phagocytic challenge [single-cell RNA-Seq]

(Submitter supplied) TREM2 is a microglial-specific gene implicated in late-onset Alzheimer's Disease (AD). Recent studies have identified that Trem2-deficient mice exhibit transcriptional changes in microglial gene expression that minimize the upregulation of lipid metabolism and lysosomal genes in AD disease models. We find that chronic phagocytic challenge from demyelination generates similiarly attenuated expression of lysosomal and lipid metabolism genes in microglia isolated from Trem2 knockout mouse brain.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
4 Samples
Download data: CSV, TXT
Series
Accession:
GSE130626
ID:
200130626
4.

TREM2 regulates microglial cholesterol metabolism upon chronic phagocytic challenge [bulk RNA-seq]

(Submitter supplied) TREM2 is a microglial-specific gene implicated in late-onset Alzheimer's Disease (AD). Recent studies have identified that Trem2-deficient mice exhibit transcriptional changes in microglial gene expression that minimize the upregulation of lipid metabolism and lysosomal genes in AD disease models. We find that chronic phagocytic challenge from demyelination generates similiarly attenuated expression of lysosomal and lipid metabolism genes in microglia isolated from Trem2 knockout mouse brain.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
74 Samples
Download data: TAB
Series
Accession:
GSE124266
ID:
200124266
5.

Expression data from WT and TREM2 deficient microglia in response to cuprizone mediated demyelination

(Submitter supplied) We examined the role of TREM2 on microglia responses to demyelination
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
10 Samples
Download data: CEL
Series
Accession:
GSE66926
ID:
200066926
6.

Transcriptomic and functional deficits in human TREM2-/- microglia impair response to Alzheimer's pathology in vivo

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
46 Samples
Download data: H5, MTX, TSV
Series
Accession:
GSE158470
ID:
200158470
7.

Transcriptomic and functional deficits in human TREM2-/- microglia impair response to Alzheimer's pathology in vivo [bulk RNA-seq]

(Submitter supplied) Bulk RNA sequencing data comparing TREM2 WT and KO microglia responses to treatment with dead neurons.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
18 Samples
Download data: H5, TSV
Series
Accession:
GSE158469
ID:
200158469
8.

Transcriptomic and functional deficits in human TREM2-/- microglia impair response to Alzheimer's pathology in vivo [scRNA-seq]

(Submitter supplied) scRNA-sequencing of human xenotransplanted microglia isogenic for TREM2 after exposure to amyloid pathology
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
4 Samples
Download data: MTX, TSV
Series
Accession:
GSE158234
ID:
200158234
9.

Transcriptomic and functional deficits in human TREM2-/- microglia impair response to Alzheimer’s pathology in vivo [RNA-seq]

(Submitter supplied) RNA-sequencing of human iPS-microglia isogenic for TREM2 after multiple treatments
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
24 Samples
Download data: TXT
10.

TREM2 Acts Downstream of CD33 in Modulating Microglial Pathology in Alzheimer's Disease

(Submitter supplied) CD33-/- and/or TREM2-/- mice were crossed with the 5xFAD mouse model of Alzheimer’s disease to generate single and double CD33/TREM2 knock-out mice on 5xFAD background. Transcriptome and gene expression analyses were performed to analyze the impact of CD33 and/or TREM2 knock-out on the transcriptome of microglia in the context of amyloid pathology. The results revealed that CD33 and/or TREM2 knock-out reprogrammed microglial gene expression signatures in 5xFAD mice in an age-dependent manner. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
73 Samples
Download data: XLSX
Series
Accession:
GSE132508
ID:
200132508
11.

TREM2 Alzheimer’s variant R47H causes similar transcriptional dysregulation to knockout, yet only subtle functional phenotypes in human iPSC-derived macrophages

(Submitter supplied) TREM2 is a microglial cell surface receptor, with risk mutations linked to Alzheimer’s disease (AD), including R47H. TREM2 signalling via SYK aids phagocytosis, chemotaxis, survival, and changes to microglial activation state. In AD mouse models, knockout (KO) of TREM2 impairs microglial clustering around amyloid, and prevents microglial activation. The R47H mutation is proposed to reduce TREM2 ligand binding. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
9 Samples
Download data: TXT
12.

Trem2 deficiency does not alter virus control but impairs phagocytic activity during neurotropic coronavirus induced demyelination

(Submitter supplied) Triggering receptor expressed on myeloid cells 2 (TREM2) plays a protective role in neurodegenerative diseases, including Alzheimer’s and demyelinating diseases. However, Trem2 functions can exacerbate tissue damage during viral respiratory or liver infections. We therefore investigated the role of TREM2 in a viral encephalomyelitis model associated with prominent Th1 responses and demyelination. To address our hypothesis, Wild type (WT) and Trem2-/- mice were infected with a sublethal glia tropic murine coronavirus (MHV-JHM) was intracranially. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL32396
30 Samples
Download data: RCC
Series
Accession:
GSE206942
ID:
200206942
13.

TREM2 is a global regulator of microglia energetic and biosynthetic metabolism during steady state and in Alzheimer’s disease

(Submitter supplied) The most common form of senile dementia, Alzheimer’s disease (AD), is characterized by Aβ plaques and neurofibrillary tangles in the CNS. AD genetic studies have identified high-risk hypomorphic variants in TREM2, a myeloid cell surface receptor that enables concerted microglial responses to Aβ plaques and neuronal cell death, including proliferation, survival, clustering and phagocytosis. How TREM2 promotes these responses is not known. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
32 Samples
Download data: TXT
Series
Accession:
GSE98563
ID:
200098563
14.

Expression data from WT and TREM2 deficient microglia in a mouse model of Alzheimer's disease

(Submitter supplied) We examined the role of TREM2 on microglia responses to amyloid-beta deposition in a mouse model of Alzheimer's disease
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
20 Samples
Download data: CEL
Series
Accession:
GSE65067
ID:
200065067
15.

TREM2 regulates microglial cell activation in response to demyelination in vivo

(Submitter supplied) Microglia are phagocytic cells that survey the brain and perform neuroprotective functions in response to tissue damage, but their activating receptors are largely unknown. Triggering receptor expressed on myeloid cells 2 (TREM2) is a microglial immunoreceptor whose loss-of-function mutations in humans cause presenile dementia, while genetic variants are associated with increased risk of neurodegenerative diseases. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL10740
18 Samples
Download data: CEL
Series
Accession:
GSE70475
ID:
200070475
16.

The TREM2-APOE pathway drives the transcriptional phenotype of dysfunctional microglia in neurodegenerative diseases VI

(Submitter supplied) Microglia play a pivotal role in the maintenance of brain homeostasis, but lose their homeostatic function during the course of neurodegenerative disorders. We identified a specific APOE-dependent molecular signature in microglia isolated from mouse models of amyotrophic lateral sclerosis, multiple sclerosis and Alzheimer’s disease (SOD1, EAE and APP-PS1) and in microglia surrounding neuritic A-plaques in human Alzheimer’s disease brain. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
39 Samples
Download data: TXT
Series
Accession:
GSE102564
ID:
200102564
17.

The TREM2-APOE pathway drives the transcriptional phenotype of dysfunctional microglia in neurodegenerative diseases V

(Submitter supplied) Microglia play a pivotal role in the maintenance of brain homeostasis, but lose their homeostatic function during the course of neurodegenerative disorders. We identified a specific APOE-dependent molecular signature in microglia isolated from mouse models of amyotrophic lateral sclerosis, multiple sclerosis and Alzheimer’s disease (SOD1, EAE and APP-PS1) and in microglia surrounding neuritic A-plaques in human Alzheimer’s disease brain. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
18 Samples
Download data: TXT
Series
Accession:
GSE102563
ID:
200102563
18.

The TREM2-APOE pathway drives the transcriptional phenotype of dysfunctional microglia in neurodegenerative diseases IV

(Submitter supplied) Microglia play a pivotal role in the maintenance of brain homeostasis, but lose their homeostatic function during the course of neurodegenerative disorders. We identified a specific APOE-dependent molecular signature in microglia isolated from mouse models of amyotrophic lateral sclerosis, multiple sclerosis and Alzheimer’s disease (SOD1, EAE and APP-PS1) and in microglia surrounding neuritic A-plaques in human Alzheimer’s disease brain. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
20 Samples
Download data: TXT
Series
Accession:
GSE102562
ID:
200102562
19.

The TREM2-APOE pathway drives the transcriptional phenotype of dysfunctional microglia in neurodegenerative diseases

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array; Expression profiling by high throughput sequencing
4 related Platforms
246 Samples
Download data: RCC
Series
Accession:
GSE101689
ID:
200101689
20.

The TREM2-APOE pathway drives the transcriptional phenotype of dysfunctional microglia in neurodegenerative diseases III

(Submitter supplied) Microglia play a pivotal role in the maintenance of brain homeostasis, but lose their homeostatic function during the course of neurodegenerative disorders. We identified a specific APOE-dependent molecular signature in microglia isolated from mouse models of amyotrophic lateral sclerosis, multiple sclerosis and Alzheimer’s disease (SOD1, EAE and APP-PS1) and in microglia surrounding neuritic A-plaques in human Alzheimer’s disease brain. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL23813
50 Samples
Download data: RCC
Series
Accession:
GSE101688
ID:
200101688
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