GEO DataSets

Identification of amyotrophic lateral sclerosis (ALS) associated genes. Post mortem spinal cord grey matter from sporadic and familial ALS patients compared with controls. Attempt to identify mechanisms by which ALS destroys motor neurons.

Organism:

Homo sapiens

Type:

Expression profiling by array, count, 3 disease state sets

Platform:

GPL80

Series:

GSE833

11 Samples

Download data

(Submitter supplied) Identification of amyotrophic lateral sclerosis (ALS) associated genes. Post mortem spinal cord grey matter from sporadic and familial ALS patients compared with controls. Keywords: other

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS412

Platform:

GPL80

11 Samples

Download data

(Submitter supplied) We used oligonucleotide microarrays to find differentially expressed genes between control subjects and those affected by sporadic amyotrophic lateral sclerosis. Keywords: disease state analysis

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL1708

20 Samples

Download data

(Submitter supplied) Transcripional profiling of lymphocytes from patients with amyotrophic lateral sclerosis (ALS) (n=11) and healthy control subjects (n=11). The goal was to determine disease response expression signatures relevant of ALS pathogenesis that affect brain and spinal cord. The reference design was used: each Cy5-labeled cRNA sample from ALS patient or healthy control subject was cohybridized on Agilent-014850 Whole Human Genome Microarray 4x44K G4112F with the reference pool formed with equal amounts of Cy3-labeled cRNAs from each sample from the healthy control group.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL4133

22 Samples

Download data: TXT

(Submitter supplied) mRNA expression in the spinal cords of the G93A-SOD1 familial ALS transgenic mouse model was compared to that in nontransgenic (Normal mouse) and transgenic mice expressing wild-type (WT)SOD1. Gene Ontology (GO)analysis was used to characterize differences in expression between G93A-SOD1 mouse and nontransgenic mouse spinal cord. Changes in multiple GO categories were found. Many of these were associated with subsystems involving cell-cell communication and intracellular signal transduction. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS1747

Platform:

GPL81

6 Samples

Download data

Analysis of spinal cord from SOD1-G93A transgenic model of amyotrophic lateral sclerosis (ALS) at 75 or 110 days of age. Cu/Zn superoxide dismutase mutations are a cause of ALS. Gene expression results, together with proteomic data, provide insight into functional changes underlying ALS progression.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 3 genotype/variation sets

Platform:

GPL81

Series:

GSE4390

6 Samples

Download data

(Submitter supplied) We report transcriptomic dysregulations in the spinal cord of asymptomatic (A: 1.5 months) symptomatic (S: 6 months) and end stage (E: 10-12 months) CHMP2Bintron5 mice by RNA sequencing. We found that genes related to immune system and lipid metabolism had altered expression levels at 1.5 month. Expression of genes related to neuronal system was atletred at 6months and expression of genes related to neuronal system and extracellular matrix xere dfound deregulated at the end-stage. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21103

32 Samples

Download data: TXT

(Submitter supplied) Familial amyotrophic lateral sclerosis (ALS) represents about 10% of ALS cases. In about 20% of familial ALS patients, a mutation in superoxide dismutase-1 (SOD1) can be found. The ubiquitous SOD1 protein converts superoxide radical anions to oxygen and hydrogen peroxide. Patients with familial ALS caused by mutations in SOD1 can show comorbidity with frontotemporal dementia and develop cognitive impairment, including apathy, inattention, verbal deficits, and hypersexuality. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL2872

32 Samples

Download data: TXT

(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

(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

(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

(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

(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

(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

(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

(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

(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

(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