| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Eike D Schomburg, Heinz Steffens, Jana Zschüntzsch, Payam Dibaj, Bernhard U Kelle. Fatigability of spinal reflex transmission in a mouse model (SOD1(G93A) ) of amyotrophic lateral sclerosis. Muscle & nerve. vol 43. issue 2. 2011-02-24. PMID:21254088. |
to analyze the progressive motor deficits during the course of this disease, we investigated fatigability and ability of recovery of spinal motor neurons by testing monosynaptic reflex transmission with increasing stimulus frequencies in the lumbar spinal cord of the sod1(g93a) mouse model for als in a comparison with wild-type (wt) mice. |
2011-02-24 |
2023-08-12 |
mouse |
| Antonello D'Arrigo, Davide Colavito, Emiliano Peña-Altamira, Michele Fabris, Mauro Dam, Antonio Contestabile, Alberta Leo. Transcriptional profiling in the lumbar spinal cord of a mouse model of amyotrophic lateral sclerosis: a role for wild-type superoxide dismutase 1 in sporadic disease? Journal of molecular neuroscience : MN. vol 41. issue 3. 2011-01-12. PMID:20177826. |
we have investigated the relationship between disease progression and altered gene expression by comparing the transcriptional profiles in lumbar spinal cord, fronto-parietal cortex and hippocampus of mutant g93a-sod1, wild-type sod1 transgenic and non-transgenic mice. |
2011-01-12 |
2023-08-12 |
mouse |
| Edor Kabashi, Jeffrey N Agar, Yu Hong, David M Taylor, Sandra Minotti, Denise A Figlewicz, Heather D Durha. Proteasomes remain intact, but show early focal alteration in their composition in a mouse model of amyotrophic lateral sclerosis. Journal of neurochemistry. vol 105. issue 6. 2010-08-13. PMID:18315558. |
our previous studies demonstrated early reduction of proteasome-mediated proteolytic activity in lumbar spinal cord of sod1(g93a) transgenic mice, tissue particularly vulnerable to disease. |
2010-08-13 |
2023-08-12 |
mouse |
| Yansu Guo, Weisong Duan, Zhongyao Li, Jing Huang, Yunxia Yin, Kunxi Zhang, Qian Wang, Zhifang Zhang, Chunyan L. Decreased GLT-1 and increased SOD1 and HO-1 expression in astrocytes contribute to lumbar spinal cord vulnerability of SOD1-G93A transgenic mice. FEBS letters. vol 584. issue 8. 2010-04-30. PMID:20303959. |
decreased glt-1 and increased sod1 and ho-1 expression in astrocytes contribute to lumbar spinal cord vulnerability of sod1-g93a transgenic mice. |
2010-04-30 |
2023-08-12 |
mouse |
| Arnaud Pambo-Pambo, Jacques Durand, Jean-Patrick Gueritau. Early excitability changes in lumbar motoneurons of transgenic SOD1G85R and SOD1G(93A-Low) mice. Journal of neurophysiology. vol 102. issue 6. 2010-02-22. PMID:19828728. |
during the second week postnatal, sod1(g93a-low) lumbar motoneurons appear more immature than those of sod1(g85r) compared with wt and we propose that different time course of the disease, possibly linked with different toxic properties of the mutated protein in each model, may explain the discrepancies between excitability changes described in the different models. |
2010-02-22 |
2023-08-12 |
mouse |
| Masatoshi Suzuki, Sandra Klein, Elizabeth A Wetzel, Michael Meyer, Jacalyn McHugh, Craig Tork, Antonio Hayes, Clive N Svendse. Acute glial activation by stab injuries does not lead to overt damage or motor neuron degeneration in the G93A mutant SOD1 rat model of amyotrophic lateral sclerosis. Experimental neurology. vol 221. issue 2. 2010-02-16. PMID:20005223. |
a longitudinal stab injury using a small knife was performed within the lumbar spinal cord region of presymptomatic sod1(g93a) rats. |
2010-02-16 |
2023-08-12 |
rat |
| Masatoshi Suzuki, Sandra Klein, Elizabeth A Wetzel, Michael Meyer, Jacalyn McHugh, Craig Tork, Antonio Hayes, Clive N Svendse. Acute glial activation by stab injuries does not lead to overt damage or motor neuron degeneration in the G93A mutant SOD1 rat model of amyotrophic lateral sclerosis. Experimental neurology. vol 221. issue 2. 2010-02-16. PMID:20005223. |
host glial activation was detected in the lumbar area surrounding a micro-knife lesion at 2 weeks after surgery in both wild type and sod1(g93a) animals. |
2010-02-16 |
2023-08-12 |
rat |
| A H Pullen, D Athanasio. Increase in presynaptic territory of C-terminals on lumbar motoneurons of G93A SOD1 mice during disease progression. The European journal of neuroscience. vol 29. issue 3. 2009-06-12. PMID:19187267. |
increase in presynaptic territory of c-terminals on lumbar motoneurons of g93a sod1 mice during disease progression. |
2009-06-12 |
2023-08-12 |
mouse |
| A H Pullen, D Athanasio. Increase in presynaptic territory of C-terminals on lumbar motoneurons of G93A SOD1 mice during disease progression. The European journal of neuroscience. vol 29. issue 3. 2009-06-12. PMID:19187267. |
prompted by our observation in spinal cords from autopsied patients suggesting selective enlargement of the ultrastructurally distinctive c-type terminal synapsing with spinal motoneurons, we examined the ultrastructural synaptology of lumbar motoneurons during disease progression in age- and sex-matched wild-type mice, transgenic g93a sod1 mice, and mice overexpressing normal human sod1 (wt(sod1)). |
2009-06-12 |
2023-08-12 |
mouse |
| Leyan Xu, David K Ryugo, Tan Pongstaporn, Karl Johe, Vassilis E Koliatso. Human neural stem cell grafts in the spinal cord of SOD1 transgenic rats: differentiation and structural integration into the segmental motor circuitry. The Journal of comparative neurology. vol 514. issue 4. 2009-05-21. PMID:19326469. |
human nscs were grafted into the lumbar protuberance of 8-week-old sod1 g93a rats; the results were compared to those on control sprague-dawley rats. |
2009-05-21 |
2023-08-12 |
human |
| Michiko Sekiya, Takashi Ichiyanagi, Yasumasa Ikeshiro, Takako Yokozaw. The Chinese prescription Wen-Pi-Tang extract delays disease onset in amyotrophic lateral sclerosis model mice while attenuating the activation of glial cells in the spinal cord. Biological & pharmaceutical bulletin. vol 32. issue 3. 2009-04-28. PMID:19252282. |
therefore, we evaluated immunohistological changes in the spinal cord of sod1(g93a) mice during the early disease period, and found that wen-pi-tang extract inhibited neuronal loss in the lumbar segment of the spinal cord of mice. |
2009-04-28 |
2023-08-12 |
mouse |
| Trent M Woodruff, Kerina J Costantini, James W Crane, Julie D Atkin, Peter N Monk, Stephen M Taylor, Peter G Noake. The complement factor C5a contributes to pathology in a rat model of amyotrophic lateral sclerosis. Journal of immunology (Baltimore, Md. : 1950). vol 181. issue 12. 2009-01-27. PMID:19050293. |
with end-stage disease, sod1(g93a) rats displayed marked deposition of c3/c3b, and a significant up-regulation of the c5ar in the lumbar spinal cord. |
2009-01-27 |
2023-08-12 |
human |
| A Vercelli, O M Mereuta, D Garbossa, G Muraca, K Mareschi, D Rustichelli, I Ferrero, L Mazzini, E Madon, F Fagiol. Human mesenchymal stem cell transplantation extends survival, improves motor performance and decreases neuroinflammation in mouse model of amyotrophic lateral sclerosis. Neurobiology of disease. vol 31. issue 3. 2008-12-15. PMID:18586098. |
we transplanted human bone marrow mesenchymal stem cells (hmscs) into the lumbar spinal cord of asymptomatic sod1(g93a) mice, an experimental model of als. |
2008-12-15 |
2023-08-12 |
mouse |
| Genevíève Gowing, Thomas Philips, Bart Van Wijmeersch, Jean-Nicolas Audet, Maarten Dewil, Ludo Van Den Bosch, An D Billiau, Wim Robberecht, Jean-Pierre Julie. Ablation of proliferating microglia does not affect motor neuron degeneration in amyotrophic lateral sclerosis caused by mutant superoxide dismutase. The Journal of neuroscience : the official journal of the Society for Neuroscience. vol 28. issue 41. 2008-11-03. PMID:18842883. |
surprisingly, a 50% reduction in reactive microglia specifically in the lumbar spinal cord of cd11b-tk(mut-30); sod1(g93a) doubly transgenic mice had no effect on motor neuron degeneration. |
2008-11-03 |
2023-08-12 |
mouse |
| Hidefumi Ito, Reika Wate, Jianhua Zhang, Shizuo Ohnishi, Satoshi Kaneko, Hisashi Ito, Satoshi Nakano, Hirofumi Kusak. Treatment with edaravone, initiated at symptom onset, slows motor decline and decreases SOD1 deposition in ALS mice. Experimental neurology. vol 213. issue 2. 2008-10-08. PMID:18718468. |
we also counted the number of lumbar motoneurons, determined the 3-nitrotyrosine/tyrosine ratio, and evaluated the abnormal sod1 aggregation in the spinal cord at the 10th day after the edaravone injection. |
2008-10-08 |
2023-08-12 |
mouse |
| Noriyuki Shibata, Motoko Kawaguchi-Niida, Tomoko Yamamoto, Sono Toi, Asao Hirano, Makio Kobayash. Effects of the PPARgamma activator pioglitazone on p38 MAP kinase and IkappaBalpha in the spinal cord of a transgenic mouse model of amyotrophic lateral sclerosis. Neuropathology : official journal of the Japanese Society of Neuropathology. vol 28. issue 4. 2008-10-07. PMID:18312546. |
to assess molecular pathological effects of the anti-inflammatory peroxisome proliferator-activated receptor-gamma (ppargamma) agonist pioglitazone in als, we verified changes in the population of neurons, astrocytes, and microglia in the ventral horns of spinal cord lumbar segments from the pioglitazone-treated and non-treated groups of mice carrying a transgene for g93a mutant human superoxide dismutase-1 (sod1) (als mice) and non-transgenic littermates (control mice), performed immunohistochemical and immunoblot analyses of ppargamma, active form of phosphorylated p38 mitogen-activated protein kinase (p-p38) and inhibitor of nuclear factor-kappab (nf-kappab)-alpha (ikappabalpha) in the spinal cords, and compared the results between the different groups. |
2008-10-07 |
2023-08-12 |
mouse |
| Angelo C Lepore, Christine Dejea, Jessica Carmen, Britta Rauck, Douglas A Kerr, Michael V Sofroniew, Nicholas J Maragaki. Selective ablation of proliferating astrocytes does not affect disease outcome in either acute or chronic models of motor neuron degeneration. Experimental neurology. vol 211. issue 2. 2008-07-07. PMID:18410928. |
while astrocytes proliferated in the lumbar spinal cord ventral horn of both disease models, they represented only a small percentage of the dividing population in the sod1(g93a) spinal cord. |
2008-07-07 |
2023-08-12 |
mouse |
| Byambasuren Dagvajantsan, Masashi Aoki, Hitoshi Warita, Naoki Suzuki, Yasuto Itoyam. Up-regulation of insulin-like growth factor-II receptor in reactive astrocytes in the spinal cord of amyotrophic lateral sclerosis transgenic rats. The Tohoku journal of experimental medicine. vol 214. issue 4. 2008-05-30. PMID:18441505. |
in this study, we investigated igf-ii receptor immunoreactivity in the anterior horns of the lumbar level of the spinal cord in sod1 transgenic rats with the h46r mutation of different ages as well as in normal littermates. |
2008-05-30 |
2023-08-12 |
human |
| Angelo C Lepore, Christine Haenggeli, Mehdi Gasmi, Kathie M Bishop, Raymond T Bartus, Nicholas J Maragakis, Jeffrey D Rothstei. Intraparenchymal spinal cord delivery of adeno-associated virus IGF-1 is protective in the SOD1G93A model of ALS. Brain research. vol 1185. 2008-03-28. PMID:17963733. |
in an effort to maximize rate of motor neuron transduction, achieve high levels of spinal igf-1 and thus enhance therapeutic benefit, we injected an adeno-associated virus 2 (aav2)-based vector encoding human igf-1 (cere-130) into lumbar spinal cord parenchyma of sod1(g93a) mice. |
2008-03-28 |
2023-08-12 |
mouse |
| Tetsuya Nagata, Hristelina Ilieva, Tetsuro Murakami, Mito Shiote, Hisashi Narai, Yasuyuki Ohta, Takeshi Hayashi, Mikio Shoji, Koji Ab. Increased ER stress during motor neuron degeneration in a transgenic mouse model of amyotrophic lateral sclerosis. Neurological research. vol 29. issue 8. 2008-03-14. PMID:17672929. |
in this study, we investigated whether er stress is involved in the pathogenesis of amyotrophic lateral sclerosis (als) using the anterior part of the lumbar spinal cord of transgenic mice carrying a mutation (g93a) in the superoxide dismutase 1 (sod1) gene. |
2008-03-14 |
2023-08-12 |
mouse |