Dataset Information


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

ABSTRACT: 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. The aim of the present study is to combine LCM and microarray analysis to compare the gene expression profiles of motor neurons from two SOD1G93A mouse strains (129Sv and C57) with different progression of the disease in order to discover the molecular mechanisms that may contribute to the distinct phenotypes and to uncover factors underlying fast and slow disease progression Motor neurons have been isolated from the spinal cord of 129SvG93A mice, C57G93A mice and non transgenic littermates at different time points and the transcription expression profile of the isolated motor neurons has been analysed


ORGANISM(S): Mus musculus  

PROVIDER: E-GEOD-46298 | ExpressionAtlas | 2015-07-16

REPOSITORIES: ExpressionAtlas

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

Nardo Giovanni G   Iennaco Raffaele R   Fusi Nicolò N   Heath Paul R PR   Marino Marianna M   Trolese Maria C MC   Ferraiuolo Laura L   Lawrence Neil N   Shaw Pamela J PJ   Bendotti Caterina C  

Brain : a journal of neurology 20130924 Pt 11

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 copy number or the burden of mutant SOD1 protein within the nervous system. We aime  ...[more]

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