| First Author | Weydt P | Year | 2004 |
| Journal | Glia | Volume | 48 |
| Issue | 2 | Pages | 179-82 |
| PubMed ID | 15378658 | Mgi Jnum | J:156055 |
| Mgi Id | MGI:4418617 | Doi | 10.1002/glia.20062 |
| Citation | Weydt P, et al. (2004) Increased cytotoxic potential of microglia from ALS-transgenic mice. Glia 48(2):179-82 |
| abstractText | Amyotrophic lateral sclerosis is a fatal, adult-onset motor neuron disease. A subset of cases is caused by mutations of superoxide dismutase 1 (SOD1) gene. The mechanisms how the mutations in this ubiquitous enzyme mediate the highly selective motor neuron degeneration, however, remain poorly understood. Recent results from transgenic animal models suggest a 'non-cell autonomous' mechanism; i.e., cells other than neurons play an active role in motor neuron death. To investigate a possible effect of mtSOD1 on microglial cells, we compared primary cultured microglia from mtSOD1-transgenic mice and nontransgenic litter controls at neonatal (3 days) and adult (60 days) age. We found that mtSOD1 expression increases the production of TNF-alpha and attenuates IL-6-release by LPS-activated adult microglia. Neonatal microglia, however, showed no differences. Our findings suggest an increased cytotoxic potential of adult mtSOD1 microglia, which only becomes apparent after microglial activation. |
