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Marked increase in cyclooxygenase-2 in ALS spinal cord: implications for therapy
K Yasojima1, W W Tourtellotte, E G McGeer
1Kinsmen Laboratory of Neurological Research, Department of Psychiatry, University of British Columbia, Vancouver, Canada.
Neurology
|September 26, 2001
Summary
Cyclooxygenase-2 (COX-2) mRNA and protein are significantly upregulated in amyotrophic lateral sclerosis (ALS) spinal cord. This finding supports potential future therapeutic strategies involving COX-2 inhibitors for ALS treatment.
Area of Science:
- Neuroscience
- Molecular Biology
- Pathology
Background:
- Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease.
- The role of cyclooxygenase-2 (COX-2) in ALS pathogenesis is not fully understood.
Purpose of the Study:
- To investigate the hypothesis that COX-2 is involved in ALS pathology.
- To quantify COX-2 mRNA levels in the spinal cord of ALS patients.
Main Methods:
- Analysis of spinal cord tissue from 11 ALS cases and 27 controls (including Alzheimer's, Parkinson's, and cerebrovascular disease).
- Reverse transcriptase-polymerase chain reaction (RT-PCR) to measure mRNA levels of COX-2, COX-1, CD11b, and cyclophilin.
- Western blot analysis to assess COX-2 protein levels.
Main Results:
- COX-2 mRNA was significantly upregulated 7.09-fold in ALS spinal cord compared to controls (p < 0.0001).
- COX-1 and microglial marker CD11b mRNA were also elevated in ALS.
- COX-2 protein levels were upregulated 3.79-fold in ALS cases (p = 0.015).
Conclusions:
- Significant upregulation of COX-2 in ALS spinal cord supports its role in the disease.
- Findings align with COX-2 upregulation observed in animal models of ALS.
- Data suggest potential therapeutic applications for COX-2 inhibitors in ALS treatment.