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Links from GEO DataSets

Items: 20

1.

Targeting miR-155 restores abnormal microglia and attenuates disease in SOD1 mice

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Other; Expression profiling by high throughput sequencing
9 related Platforms
118 Samples
Download data: RCC, TXT
Series
Accession:
GSE52947
ID:
200052947
2.

MG447 profile of lumbar spinal cord homogenate from healthy controls and ALS

(Submitter supplied) Amyotrophic lateral sclerosis (ALS) is a paralytic degenerative disease of the nervous system. In the SOD1 mouse model of ALS we found loss of the molecular and functional microglia signature associated with pronounced expression of miR-155 in SOD1 mice. We also found increased expression of miR-155 in the spinal cord of ALS subjects. Genetic ablation of miR-155 increased survival in SOD1 mice and reversed the abnormal microglial and monocyte molecular signature. more...
Organism:
Homo sapiens
Type:
Other
Platform:
GPL18023
16 Samples
Download data: RCC
Series
Accession:
GSE52959
ID:
200052959
3.

miR-155 plays a crucial role in ALS and is an immune therapeutic target [RNA-Seq]

(Submitter supplied) Amyotrophic lateral sclerosis (ALS) is a paralytic degenerative disease of the nervous system. In the SOD1 mouse model of ALS we found loss of the molecular and functional microglia signature associated with pronounced expression of miR-155 in SOD1 mice. We also found increased expression of miR-155 in the spinal cord of ALS subjects. Genetic ablation of miR-155 increased survival in SOD1 mice and reversed the abnormal microglial and monocyte molecular signature. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
20 Samples
Download data: TXT
4.

miRNA profile in lumbar spinal cord homogenate of SOD-miR155 Tg mice

(Submitter supplied) Amyotrophic lateral sclerosis (ALS) is a paralytic degenerative disease of the nervous system. In the SOD1 mouse model of ALS we found loss of the molecular and functional microglia signature associated with pronounced expression of miR-155 in SOD1 mice. We also found increased expression of miR-155 in the spinal cord of ALS subjects. Genetic ablation of miR-155 increased survival in SOD1 mice and reversed the abnormal microglial and monocyte molecular signature. more...
Organism:
Mus musculus
Type:
Other
Platform:
GPL18014
6 Samples
Download data: RCC
Series
Accession:
GSE52898
ID:
200052898
5.

MG400 profile of microglia from SOD miR155-KO mice

(Submitter supplied) Amyotrophic lateral sclerosis (ALS) is a paralytic degenerative disease of the nervous system. In the SOD1 mouse model of ALS we found loss of the molecular and functional microglia signature associated with pronounced expression of miR-155 in SOD1 mice. We also found increased expression of miR-155 in the spinal cord of ALS subjects. Genetic ablation of miR-155 increased survival in SOD1 mice and reversed the abnormal microglial and monocyte molecular signature. more...
Organism:
Mus musculus
Type:
Other
Platform:
GPL18002
6 Samples
Download data: RCC
Series
Accession:
GSE52803
ID:
200052803
6.

Inflammation gene profile of sc-microglia in SOD mice

(Submitter supplied) Amyotrophic lateral sclerosis (ALS) is a paralytic degenerative disease of the nervous system. In the SOD1 mouse model of ALS we found loss of the molecular and functional microglia signature associated with pronounced expression of miR-155 in SOD1 mice. We also found increased expression of miR-155 in the spinal cord of ALS subjects. Genetic ablation of miR-155 increased survival in SOD1 mice and reversed the abnormal microglial and monocyte molecular signature. more...
Organism:
Mus musculus
Type:
Other
Platform:
GPL17981
14 Samples
Download data: RCC
Series
Accession:
GSE52673
ID:
200052673
7.

Immune gene profile in lumbar spinal cord homogenate of healthy controls and ALS

(Submitter supplied) Amyotrophic lateral sclerosis (ALS) is a paralytic degenerative disease of the nervous system. In the SOD1 mouse model of ALS we found loss of the molecular and functional microglia signature associated with pronounced expression of miR-155 in SOD1 mice. We also found increased expression of miR-155 in the spinal cord of ALS subjects. Genetic ablation of miR-155 increased survival in SOD1 mice and reversed the abnormal microglial and monocyte molecular signature. more...
Organism:
Homo sapiens
Type:
Other
Platform:
GPL17980
20 Samples
Download data: RCC
Series
Accession:
GSE52672
ID:
200052672
8.

MG400 profile of spinal cord microglia during disease progression in SOD mice

(Submitter supplied) Amyotrophic lateral sclerosis (ALS) is a paralytic degenerative disease of the nervous system. In the SOD1 mouse model of ALS we found loss of the molecular and functional microglia signature associated with pronounced expression of miR-155 in SOD1 mice. We also found increased expression of miR-155 in the spinal cord of ALS subjects. Genetic ablation of miR-155 increased survival in SOD1 mice and reversed the abnormal microglial and monocyte molecular signature. more...
Organism:
Mus musculus
Type:
Other
Platform:
GPL17979
10 Samples
Download data: RCC
Series
Accession:
GSE52671
ID:
200052671
9.

miRNA profile in lumbar spinal cord homogenate from healthy controls and ALS

(Submitter supplied) Amyotrophic lateral sclerosis (ALS) is a paralytic degenerative disease of the nervous system. In the SOD1 mouse model of ALS we found loss of the molecular and functional microglia signature associated with pronounced expression of miR-155 in SOD1 mice. We also found increased expression of miR-155 in the spinal cord of ALS subjects. Genetic ablation of miR-155 increased survival in SOD1 mice and reversed the abnormal microglial and monocyte molecular signature. more...
Organism:
Homo sapiens
Type:
Other
Platform:
GPL17978
20 Samples
Download data: RCC
Series
Accession:
GSE52670
ID:
200052670
10.

miRNA profile in SOD-155 microglia

(Submitter supplied) Amyotrophic lateral sclerosis (ALS) is a paralytic degenerative disease of the nervous system. In the SOD1 mouse model of ALS we found loss of the molecular and functional microglia signature associated with pronounced expression of miR-155 in SOD1 mice. We also found increased expression of miR-155 in the spinal cord of ALS subjects. Genetic ablation of miR-155 increased survival in SOD1 mice and reversed the abnormal microglial and monocyte molecular signature. more...
Organism:
Mus musculus
Type:
Other
Platform:
GPL17873
6 Samples
Download data: RCC
Series
Accession:
GSE52668
ID:
200052668
11.

Amyotrophic lateral sclerosis

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by array; Non-coding RNA profiling by array
Platforms:
GPL15846 GPL15847
48 Samples
Download data: TXT
Series
Accession:
GSE39644
ID:
200039644
12.

NanoString miRNA profiling of peripheral blood sorted CD14+CD16- monocytes from amyotrophic lateral sclerosis, multiple sclerosis and healthy control subjects

(Submitter supplied) We investigated the innate immune system in the SOD1 ALS model. We found that splenic Ly6CHi monocytes were activated and their progressive recruitment to the spinal cord, but not brain, correlated with neuronal loss. We found a decrease in resident microglia in the spinal cord with disease progression. Two months prior to disease onset, splenic Ly6CHi monocytes had an M1 signature which included increased CCR2. more...
Organism:
Homo sapiens
Type:
Non-coding RNA profiling by array
Platform:
GPL15847
24 Samples
Download data: TXT
Series
Accession:
GSE39643
ID:
200039643
13.

NanoString nCounter immune-related gene expression in blood sorted CD14+CD16- monocytes from sALS, fALS and HC subjects

(Submitter supplied) We investigated the innate immune system in the SOD1 ALS model. We found that splenic Ly6CHi monocytes were activated and their progressive recruitment to the spinal cord, but not brain, correlated with neuronal loss. We found a decrease in resident microglia in the spinal cord with disease progression. Two months prior to disease onset, splenic Ly6CHi monocytes had an M1 signature which included increased CCR2. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL15846
24 Samples
Download data: TXT
Series
Accession:
GSE39642
ID:
200039642
14.

Microglia-specific microarray analysis at early symptomatic age in a mouse model of amyotrophic lateral sclerosis

(Submitter supplied) Microarray analysis of microglia in a mouse model of amyotrophic lateral sclerosis identified the dysregulation of Brca1.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
6 Samples
Download data: CEL
Series
Accession:
GSE96047
ID:
200096047
15.

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
16.

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
17.

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
18.

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
19.

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
20.

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

(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:
GPL23812
56 Samples
Download data: RCC
Series
Accession:
GSE101687
ID:
200101687
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