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Links from GEO DataSets

Items: 9

1.
Full record GDS1747

SOD1-G93A transgenic model of amyotrophic lateral sclerosis: spinal cord

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
DataSet
Accession:
GDS1747
ID:
1747
2.

Analysis of expression in SOD1 transgenic mouse spinal cord

(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
Series
Accession:
GSE4390
ID:
200004390
3.

Whole genome transcriptome analysis identifies indices of fast and slow disease progression in two ALS mouse models

(Submitter supplied) Microarray analysis has been applied to the study of ALS in order to investigate gene expression in whole spinal cord homogenates of SOD1 G93A mice and human ALS cases, although the massive presence of glial cells and inflammatory factors has made it difficult to define which gene expression changes were motor neuron specific. Recently, laser capture microdissection (LCM), combined with microarray analysis, has allowed the identification of motor neuron specific changes in gene expression in mouse and human ALS cases. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
64 Samples
Download data: CEL
Series
Accession:
GSE46298
ID:
200046298
4.

LCM-based microarray analysis of TAU-P301L and SOD1-G93A motor neurons and surrounding glial cells

(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
Series
Accession:
GSE22482
ID:
200022482
5.

Single-cell RNA-seq analysis of the brainstem of mutant SOD1 mice reveals perturbed cell types and pathways of amyotrophic lateral sclerosis

(Submitter supplied) Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease in which motor neurons throughout the brain and spinal cord progressively degenerate resulting in muscle atrophy, paralysis and death. Recent studies using animal models of ALS implicate multiple cell-types (e.g., astrocytes and microglia) in ALS pathogenesis in the spinal motor systems. To ascertain cellular vulnerability and cell-type specific mechanisms of ALS in the brainstem that orchestrates oral-motor functions, we conducted parallel single cell RNA sequencing (scRNA-seq) analysis using the high-throughput Drop-seq method. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
4 Samples
Download data: TAR
Series
Accession:
GSE178693
ID:
200178693
6.

Signaling pathways in skeletal muscle of Amyotrophic Lateral Sclerosis mouse model

(Submitter supplied) Gene expression analyses through cDNA microarray of fifteen gastrocnemius muscles from transgenic and wild-type SOD1G93A mouse model by the ages of 40 and 80 days old were performed. We used a customized cDNA array containing the cDNA platform comprised of 2352 spots, 326 of them orthologous to mouse, 1384 additional human cDNA sequences, 496 negative controls (DMSO) and 48 positive controls (the Q gene from λ-phage). more...
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by array
Platform:
GPL9692
15 Samples
Download data
Series
Accession:
GSE40328
ID:
200040328
7.

Early alterations in lipid metabolism in the spinal cord of SOD1 mice

(Submitter supplied) Amyotrophic lateral sclerosis (ALS) is a multifactorial and complex fatal degenerative disorder. A number of pathological mechanisms that lead to motor neuron death have been identified, although there are many unknowns in the disease aetiology of ALS. Alterations in lipid metabolism are well documented in the progression of ALS, both at the systemic level and in the spinal cord of mouse models and ALS patients. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
10 Samples
Download data: CSV
Series
Accession:
GSE184484
ID:
200184484
8.

Amyotrophic lateral sclerosis

(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
Series
Accession:
GSE833
ID:
200000833
9.
Full record GDS412

Amyotrophic lateral sclerosis (Lou Gehrig's Disease)

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
DataSet
Accession:
GDS412
ID:
412
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