Abstract
Amyotrophic lateral sclerosis (ALS) is a devastating motor neuron disease. One mechanism involved in ALS pathology is neuroinflammation. Neuroinflammation is mediated by soluble pro-inflammatory molecules such as cytokines, prostaglandins and nitric oxide. Studies on transgenic mice demonstrated the expression of pro-inflammatory mediators in early stages of murine ALS. Recently a transgenic rat model became available. Since species differences in regard to cytokine expression have been reported in other disease models we set out to validate the neuroinflammatory hypothesis in the ALS-transgenic rat. We investigated the expression of inflammatory mediators and growth factors in the spinal cord by semi-quantitative RT-PCR. We found that several pro-inflammatory mediators are up-regulated at asymptomatic and end-stages, whereas VEGF, a neuroprotective factor was down-regulated.
Original language | English (US) |
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Pages (from-to) | 2513-2516 |
Number of pages | 4 |
Journal | Neuroreport |
Volume | 15 |
Issue number | 16 |
DOIs | |
State | Published - Dec 15 2004 |
Keywords
- Amyotrophic lateral sclerosis
- Cytokines
- G93A SOD1 rat
- Microglia
- Neuroinflammation; VEGF
ASJC Scopus subject areas
- General Neuroscience