Analysis of the superoxide dismutase 1 (SOD1)-dependent transcriptome in mouse oculomotor nucleus and spinal cord

2019 ◽  
Author(s):  
CA McMullen
Keyword(s):  
Spinal Cord ◽  
Superoxide Dismutase ◽  
Superoxide Dismutase 1 ◽  
Oculomotor Nucleus

Multilayer polyion complex nanoformulations of superoxide dismutase 1 for acute spinal cord injury

2018 ◽  
Vol 270 ◽  
pp. 226-236 ◽  
Author(s):  
N.V. Nukolova ◽  
A.D. Aleksashkin ◽  
T.O. Abakumova ◽  
A.Y. Morozova ◽  
I.L. Gubskiy ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Superoxide Dismutase ◽  
Acute Spinal Cord Injury ◽  
Superoxide Dismutase 1 ◽  
Polyion Complex ◽  
Cord Injury

scholarly journals Genetic model of motor neuron disease in B6SJL-Tg mice: new data on the dynamics of motor symptoms and immunohistochemical manifestations of the neurodegenerative process

2020 ◽  
Vol 10 (3) ◽  
pp. 63-73
Author(s):  
А. V. Stavrovskaya ◽  
D. N. Voronkov ◽  
E. A. Artyomova ◽  
B. V. Belugin ◽  
М. М. Shmarov ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Superoxide Dismutase ◽  
Motor Neuron ◽  
Motor Neuron Disease ◽  
Morphological Changes ◽  
New Drugs ◽  
Mutant Form ◽  
Superoxide Dismutase 1 ◽  
Neurodegenerative Process ◽  
Familial Form

Introduction. Over the past several decades, the study of mutations associated with motor neuron disease has led to the development of a number of transgenic animal models of motor neuron disease. One of the causes of the familial form of this disorder is mutations in the gene encoding Cu/Zn superoxide dismutase 1. The B6SJL-Tg (SOD1*G93A) mouse strain expresses a mutant form of human superoxide dismutase 1. Aim of study. To assess motor functions, dynamics of survival, and morphological changes in the spinal cord of transgenic B6SJL-Tg (SOD1*G93A) mice. Material and methods. In total, 31 animals have been studied. Starting from the age of 22 weeks, once every two weeks, the “open field” and “beam walking” motor tests were performed. The morphological changes in the spinal cord were evaluated at intermediate (26–35 weeks) and late stages (40–45 weeks). Neuronal proteins NeuN and PGP9.5, gliofibrillar protein, cyclonucleotide phosphatase (a marker of oligodendroglia) and a marker protein of microglia IBA1 were detected by immunohistochemistry; antibodies MTC02 to the outer membrane protein were used to detect mitochondria. Results. Motor problems appeared at the age of 24–26 weeks and steadily progressed; one could see consistent paresis of the hindlimbs, then the forelimbs, which was accompanied by general hypotrophy of the animals. There was a greater variability in the timing of symptom onset and life expectancy in males compared to females. The neurodegenerative process with damage to motor neurons was accompanied by the activation of micro- and astroglia. A sharp decrease in immunoreactivity to the mitochondrial marker MTC02 was found. Conclusion. The obtained results demonstrate new details of the development of a complex of motor and pathomorphological changes characteristic of motor neuron disease in B6SJL-Tg (SOD1*G93A) mice. Clarification of the fine dynamics of the neurodegenerative process in these animals is of great importance for monitoring the course of the disease during preclinical trials of new drugs and methods of gene therapy.

Correction of humoral derangements from mutant superoxide dismutase 1 spinal cord

2006 ◽  
Vol 60 (6) ◽  
pp. 716-728 ◽  
Author(s):  
Yun-Sook Kim ◽  
Tara Martinez ◽  
Deepa M. Deshpande ◽  
Jennifer Drummond ◽  
Katie Provost-Javier ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Superoxide Dismutase ◽  
Superoxide Dismutase 1
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