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Academic literature on the topic 'SOD1G85R mouse'
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Journal articles on the topic "SOD1G85R mouse"
Leyton-Jaimes, Marcel F., Clara Benaim, Salah Abu-Hamad, Joy Kahn, Amos Guetta, Richard Bucala, and Adrian Israelson. "Endogenous macrophage migration inhibitory factor reduces the accumulation and toxicity of misfolded SOD1 in a mouse model of ALS." Proceedings of the National Academy of Sciences 113, no. 36 (August 22, 2016): 10198–203. http://dx.doi.org/10.1073/pnas.1604600113.
Full textPambo-Pambo, Arnaud, Jacques Durand, and Jean-Patrick Gueritaud. "Early Excitability Changes in Lumbar Motoneurons of Transgenic SOD1G85R and SOD1G93A-Low Mice." Journal of Neurophysiology 102, no. 6 (December 2009): 3627–42. http://dx.doi.org/10.1152/jn.00482.2009.
Full textBK, Binukumar, Susan Skuntz, Michaela Prochazkova, Sashi Kesavapany, Niranjana D. Amin, Varsha Shukla, Philip Grant, Ashok B. Kulkarni, and Harish C. Pant. "Overexpression of the Cdk5 inhibitory peptide in motor neurons rescue of amyotrophic lateral sclerosis phenotype in a mouse model." Human Molecular Genetics 28, no. 19 (May 9, 2019): 3175–87. http://dx.doi.org/10.1093/hmg/ddz118.
Full textRobertson, Janice, Mohammad M. Doroudchi, Minh Dang Nguyen, Heather D. Durham, Michael J. Strong, Gerry Shaw, Jean-Pierre Julien, and Walter E. Mushynski. "A neurotoxic peripherin splice variant in a mouse model of ALS." Journal of Cell Biology 160, no. 6 (March 17, 2003): 939–49. http://dx.doi.org/10.1083/jcb.200205027.
Full textMarques, Christine, Thibaut Burg, Jelena Scekic-Zahirovic, Mathieu Fischer, and Caroline Rouaux. "Upper and Lower Motor Neuron Degenerations Are Somatotopically Related and Temporally Ordered in the Sod1 Mouse Model of Amyotrophic Lateral Sclerosis." Brain Sciences 11, no. 3 (March 13, 2021): 369. http://dx.doi.org/10.3390/brainsci11030369.
Full textKang, Jihong, and Serge Rivest. "MyD88-deficient bone marrow cells accelerate onset and reduce survival in a mouse model of amyotrophic lateral sclerosis." Journal of Cell Biology 179, no. 6 (December 17, 2007): 1219–30. http://dx.doi.org/10.1083/jcb.200705046.
Full textFilali, Mohammed, Robert Lalonde, and Serge Rivest. "Sensorimotor and cognitive functions in a SOD1G37R transgenic mouse model of amyotrophic lateral sclerosis." Behavioural Brain Research 225, no. 1 (November 2011): 215–21. http://dx.doi.org/10.1016/j.bbr.2011.07.034.
Full textMartineau, Éric, Danielle Arbour, Joanne Vallée, and Richard Robitaille. "Properties of Glial Cell at the Neuromuscular Junction Are Incompatible with Synaptic Repair in the SOD1G37R ALS Mouse Model." Journal of Neuroscience 40, no. 40 (August 28, 2020): 7759–77. http://dx.doi.org/10.1523/jneurosci.1748-18.2020.
Full textMaier, Marcel, Tobias Welt, Fabian Wirth, Fabio Montrasio, Daniel Preisig, Jordan McAfoose, Fernando G. Vieira, et al. "A human-derived antibody targets misfolded SOD1 and ameliorates motor symptoms in mouse models of amyotrophic lateral sclerosis." Science Translational Medicine 10, no. 470 (December 5, 2018): eaah3924. http://dx.doi.org/10.1126/scitranslmed.aah3924.
Full textHilton, James B., Kai Kysenius, Anthony R. White, and Peter J. Crouch. "The accumulation of enzymatically inactive cuproenzymes is a CNS-specific phenomenon of the SOD1G37R mouse model of ALS and can be restored by overexpressing the human copper transporter hCTR1." Experimental Neurology 307 (September 2018): 118–28. http://dx.doi.org/10.1016/j.expneurol.2018.06.006.
Full textDissertations / Theses on the topic "SOD1G85R mouse"
Pambo-Pambo, Arnaud Brice. "Etude du développement postnatal des motoneurones lombaires de deux souches de souris transgéniques, modèles de la sclérose latérale amyotrophique." Thesis, Aix-Marseille 2, 2010. http://www.theses.fr/2010AIX20716.
Full textThe SOD1 murine models of Amyotrophic Lateral Sclerosis (ALS) allowed major progress in the understanding of mechanisms which could lead to a selective loss of motoneurons (Mns), but these models display differences in the severity and time course of the disease. Changes in intrinsic properties of motoneurons may induce changes in excitability and intracellular calcium homeostasis leading to motoneuron death.Therefore, we studied electrophysiological properties of lumbar Mns from SOD1G85R and SOD1G93A mice, low expressor lines, during the first two postnatal weeks in order to identify possible early presymptomatic abnormalities. Our studies were carried out on two in vitro preparations: the whole isolated spinal cord and acute spinal cord slices. Mutant Mns display, in the two preparations, a modified action potential characterized by an increased duration due to a decrease of the maximal speeds of depolarisation and repolarisation and a reduction of the spike amplitude. These alterations appeared between P2-P5 in SOD1G85R Mns and between P6-P10 in SOD1G93A Mns and suggest a decrease of the density of sodium and potassium channels related to action potential. We also showed on spinal cord slices between P6-P10 that the gain of frequency decreases for SOD1G85R Mns and increases for SOD1G93A Mns without any change in the density of persistent inward sodium or calcium currents in these different mutant Mns. We observed also that the resting membrane potential of SOD1G93A Mns on spinal cord slices is decreased. The membrane properties of SOD1G85R Mns between P6-P10 were less susceptible to changes in presence of an extracellular calcium overload. Differential effects of this extracellular calcium overload on membrane properties of WT and SOD1G85R Mns could be due to different alterations of the potential dependence of voltage-gated channels and/or to the modulation of some types of channels sensitive to extracellular calcium. An over-branching of dendritic arborization, similar to that previously described in SOD1G85R Mns, was observed in SOD1G93A at P8-P9 with the above-mentioned action potential alterations and a weak rheobasic current. These morphogical and electrical changes could indicate together alterations of kinetics and/or density of channels on different sites on these Mns. In conclusion, our work shows on one hand that SOD1G85R and SOD1G93A mutations induce similar alterations of lumbar Mns properties but time-shifted in these two murine models and on the other hand that some alterations seem to be specific to a given SOD1 mutation