Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Transcriptomic indices of fast and slow disease progression in two mouse models of amyotrophic lateral sclerosis.

Brain : a journal of neurology - 1 Nov 2013

Nardo Giovanni, Iennaco Raffaele, Fusi Nicolò, Heath Paul R, Marino Marianna, Trolese Maria C, Ferraiuolo Laura, Lawrence Neil, Shaw Pamela J, Bendotti Caterina

Abstract excerpt

Amyotrophic lateral sclerosis is heterogeneous with high variability in the speed of progression even in cases with a defined genetic cause such as superoxide dismutase 1 (SOD1) mutations. We reported that SOD1(G93A) mice on distinct genetic backgrounds (C57 and 129Sv) show consistent phenotypic differences in speed of disease progression and life-span that are not explained by differences in human SOD1 transgene...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Amyotrophic Lateral Sclerosis
Share to Disease Progression

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Mice, 129 Strain

Share to Mice, Transgenic

Share to Motor Neurons

Share to Superoxide Dismutase

Share to Superoxide Dismutase-1

Share to Transcriptome

Source

Identifiers

PMID: 24065725
DOI: 10.1093/brain/awt250

Genes

SOD1

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Transcriptomic indices of fast and slow disease progression in two mouse models of amyotrophic lateral sclerosis.PMID 24065725Read ↗

Microarray Analysis of the Cellular Pathways Involved in the Adaptation to and Progression of Motor Neuron Injury in the SOD1 G93A Mouse Model of Familial ALSSemantic proximity Read ↗

Early gene expression changes in spinal cord from SOD1G93A Amyotrophic Lateral Sclerosis animal modelSemantic proximity Read ↗

New Insights on the Mechanisms of Disease Course Variability in ALS from Mutant SOD1 Mouse Models.Semantic proximity Read ↗

Identification of B6SJL mSOD1(G93A) mouse subgroups with different disease progression rates.Semantic proximity Read ↗

Differences in protein quality control correlate with phenotype variability in 2 mouse models of familial amyotrophic lateral sclerosis.Semantic proximity Read ↗

Unraveling the Complexity of Amyotrophic Lateral Sclerosis: Recent Advances from the Transgenic Mutant SOD1 MiceSemantic proximity Read ↗

Integrative gene-tissue microarray-based approach for identification of human disease biomarkers: application to amyotrophic lateral sclerosis.Semantic proximity Read ↗

Up-regulation of cholesterol synthesis pathways and limited neurodegeneration in a knock-in <i>Sod1</i> mutant mouse model of ALSSemantic proximity Read ↗

Transcriptional modulation unique to vulnerable motor neurons predicts ALS across species and SOD1 mutations.Semantic proximity Read ↗

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

Tissue-enhanced plasma proteomic analysis for disease stratification in amyotrophic lateral sclerosisSemantic proximity Read ↗

Transcriptional modulation unique to vulnerable motor neurons predicts ALS across species and SOD1 mutationsSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.