| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Bradley J Turner, Elizabeth C Lopes, Surindar S Cheem. Neuromuscular accumulation of mutant superoxide dismutase 1 aggregates in a transgenic mouse model of familial amyotrophic lateral sclerosis. Neuroscience letters. vol 350. issue 2. 2003-11-06. PMID:12972170. |
a progressive age-dependent increase in mutant sod1 level, aggregation and stabilisation by cross-species heterodimers was determined in lumbar spinal cord, sciatic nerve and gastrocnemius muscle. |
2003-11-06 |
2023-08-12 |
mouse |
| D W Zang, S S Cheem. Degeneration of corticospinal and bulbospinal systems in the superoxide dismutase 1(G93A G1H) transgenic mouse model of familial amyotrophic lateral sclerosis. Neuroscience letters. vol 332. issue 2. 2002-11-26. PMID:12384220. |
in the superoxide dismutase 1 (sod1)(g93a g1h) transgenic mouse, the primary pathology and disease signs are associated with the degeneration of motor neurons in the lumbar spinal cord. |
2002-11-26 |
2023-08-12 |
mouse |
| Fiona M Menzies, Andrew J Grierson, Mark R Cookson, Paul R Heath, Janine Tomkins, Denise A Figlewicz, Paul G Ince, Pamela J Sha. Selective loss of neurofilament expression in Cu/Zn superoxide dismutase (SOD1) linked amyotrophic lateral sclerosis. Journal of neurochemistry. vol 82. issue 5. 2002-10-18. PMID:12358759. |
here we have used microdissected lumbar spinal cord motor neurones from human sod1 fals patients as well as g93a sod1 transgenic mice and demonstrated that reduced nfl mrna levels are seen in both. |
2002-10-18 |
2023-08-12 |
mouse |
| David S Howland, Jian Liu, Yijin She, Beth Goad, Nicholas J Maragakis, Benjamin Kim, Jamie Erickson, John Kulik, Lisa DeVito, George Psaltis, Louis J DeGennaro, Don W Cleveland, Jeffrey D Rothstei. Focal loss of the glutamate transporter EAAT2 in a transgenic rat model of SOD1 mutant-mediated amyotrophic lateral sclerosis (ALS). Proceedings of the National Academy of Sciences of the United States of America. vol 99. issue 3. 2002-03-07. PMID:11818550. |
pathological abnormalities included vacuoles initially in the lumbar spinal cord and subsequently in more cervical areas, along with inclusion bodies that stained for sod1, hsp70, neurofilaments, and ubiquitin. |
2002-03-07 |
2023-08-12 |
mouse |
| M F Azari, A Galle, E C Lopes, J Kurek, S S Cheem. Leukemia inhibitory factor by systemic administration rescues spinal motor neurons in the SOD1 G93A murine model of familial amyotrophic lateral sclerosis. Brain research. vol 922. issue 1. 2002-02-19. PMID:11730713. |
in this study we investigated whether intense systemic lif therapy prevents the loss of lumbar motoneurons in the transgenic sod1 g93a mouse model of familial amyotrophic lateral sclerosis. |
2002-02-19 |
2023-08-12 |
mouse |
| M Azzouz, W Krezel, P Dollé, C Vodouhe, J M Warter, P Poindron, J Bor. Compensatory mechanism of motor defect in SOD1 transgenic mice by overactivation of striatal cholinergic neurons. Neuroreport. vol 10. issue 5. 1999-06-23. PMID:10321477. |
transgenic mice over-expressing the human sod1 gene containing a gly-->ala substitution at position 93 (g93a) were employed to explore the effects of the sod1 mutation on choline acetyltransferase (chat) expression in the striatum, and in the lumbar and cervical spinal cord. |
1999-06-23 |
2023-08-12 |
mouse |
| P K Andrus, T J Fleck, M E Gurney, E D Hal. Protein oxidative damage in a transgenic mouse model of familial amyotrophic lateral sclerosis. Journal of neurochemistry. vol 71. issue 5. 1998-11-30. PMID:9798929. |
in the present study, we analyzed the extent of oxidative injury to lumbar and cervical spinal cord proteins in transgenic fals mice that overexpress the sod1 mutation [tgn(sod1-g93a)g1h] in comparison with nontransgenic mice. |
1998-11-30 |
2023-08-12 |
mouse |
| E D Hall, P K Andrus, J A Oostveen, T J Fleck, M E Gurne. Relationship of oxygen radical-induced lipid peroxidative damage to disease onset and progression in a transgenic model of familial ALS. Journal of neuroscience research. vol 53. issue 1. 1998-09-24. PMID:9670993. |
transgenic mice that overexpress a mutated human cuzn superoxide dismutase (sod1) gene (gly93-->ala) found in some patients with familial als (fals) have been shown to develop motor neuron disease, as evidenced by motor neuron loss in the lumbar and cervical spinal regions and a progressive loss of voluntary motor activity. |
1998-09-24 |
2023-08-12 |
mouse |
| E D Hall, J A Oostveen, M E Gurne. Relationship of microglial and astrocytic activation to disease onset and progression in a transgenic model of familial ALS. Glia. vol 23. issue 3. 1998-08-27. PMID:9633809. |
transgenic mice that highly over-express a mutated human cuzn superoxide dismutase (sod1) gene [gly93-->ala; tgn(sod1-g93a)g1h line] found in some patients with familial als (fals) have been shown to develop motor neuron disease that is characterized by motor neuron loss in the lumbar and cervical spinal regions and a progressive loss of motor activity. |
1998-08-27 |
2023-08-12 |
mouse |