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Physiol. Genomics (November 25, 2003). doi:10.1152/physiolgenomics.00087.2001 Free Article
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Submitted on September 27, 2001
Accepted on November 14, 2003

The molecular signature of late-stage human ALS revealed by expression profiling of post-mortem spinal cord gray matter

Fernando Dangond1, Daehee Hwang2, Sandra Camelo1, Piera Pasinelli3, Matthew P Frosch4, Gregory Stephanopoulos2, George Stephanopoulos2, Robert H Brown, Jr.3, and Steven R Gullans1*

1 Neurology, Brigham and Women's Hospital, Boston, MA, USA
2 Chemical Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA
3 Neurology, Massachusetts General Hospital, Boston, MA, USA
4 Neuropathology, Massachusetts General Hospital, Boston, MA, USA

* To whom correspondence should be addressed. E-mail: sgullans{at}rics.bwh.harvard.edu.

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 approximately 6,800 genes in post-mortem 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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