Journal
PHYSIOLOGICAL GENOMICS
Volume 16, Issue 2, Pages 229-239Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/physiolgenomics.00087.2001
Keywords
amyotrophic lateral sclerosis; DNA microarrays; mitochondria; excitotoxicity; apoptosis
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Funding
- NCI NIH HHS [1K08-CA-80084] Funding Source: Medline
- NINDS NIH HHS [1PO-NS-31248, R01-NS-37812, R21-NS-41623, 1P50-NS-38375] Funding Source: Medline
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Little is known about global gene expression patterns in the human neurodegenerative disease amyotrophic lateral sclerosis (ALS). To address this, we used high-density oligonucleotide microarray technology to compare expression levels of similar to6,800 genes in postmortem spinal cord gray matter obtained from individuals with ALS as well as normal individuals. Using Fisher discriminant analysis (FDA) and leave-one-out cross-validation (LOOCV), we discerned an ALS-specific signature. Moreover, it was possible to distinguish familial ALS (FALS) from sporadic ALS (SALS) gene expression profiles. Characterization of the specific genes significantly altered in ALS uncovered a pro-inflammatory terminal state. Moreover, we found alterations in genes involved in mitochondrial function, oxidative stress, excitotoxicity, apoptosis, cytoskeletal architecture, RNA transcription and translation, proteasomal function, and growth and signaling. It is apparent from this study that DNA microarray analysis and appropriate bioinformatics can reveal distinct phenotypic changes that underlie the terminal stages of neurodegeneration in ALS.
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