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Article ; Online: Ex vivo gene therapy for the treatment of neurological disorders.

Gowing, Genevieve / Svendsen, Soshana / Svendsen, Clive N

2017 Volume 230, Page(s) 99–132

Abstract: Ex vivo gene therapy involves the genetic modification of cells outside of the body to produce therapeutic factors and their subsequent transplantation back into patients. Various cell types can be genetically engineered. However, with the explosion in ... ...

Abstract	Ex vivo gene therapy involves the genetic modification of cells outside of the body to produce therapeutic factors and their subsequent transplantation back into patients. Various cell types can be genetically engineered. However, with the explosion in stem cell technologies, neural stem/progenitor cells and mesenchymal stem cells are most often used. The synergy between the effect of the new cell and the additional engineered properties can often provide significant benefits to neurodegenerative changes in the brain. In this review, we cover both preclinical animal studies and clinical human trials that have used ex vivo gene therapy to treat neurological disorders with a focus on Parkinson's disease, Huntington's disease, Alzheimer's disease, ALS, and stroke. We highlight some of the major advances in this field including new autologous sources of pluripotent stem cells, safer ways to introduce therapeutic transgenes, and various methods of gene regulation. We also address some of the remaining hurdles including tunable gene regulation, in vivo cell tracking, and rigorous experimental design. Overall, given the current outcomes from researchers and clinical trials, along with exciting new developments in ex vivo gene and cell therapy, we anticipate that successful treatments for neurological diseases will arise in the near future.
MeSH term(s)	Animals ; Cell- and Tissue-Based Therapy ; Genetic Therapy ; Humans ; Mesenchymal Stem Cell Transplantation ; Nervous System Diseases/genetics ; Nervous System Diseases/therapy ; Neural Stem Cells ; Stem Cell Transplantation
Language	English
Publishing date	2017
Publishing country	Netherlands
Document type	Journal Article ; Review
ISSN	1875-7855 ; 0079-6123
ISSN (online)	1875-7855
ISSN	0079-6123
DOI	10.1016/bs.pbr.2016.11.003
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: A cGMP-applicable expansion method for aggregates of human neural stem and progenitor cells derived from pluripotent stem cells or fetal brain tissue.

Shelley, Brandon C / Gowing, Geneviève / Svendsen, Clive N

Journal of visualized experiments : JoVE

2014 , Issue 88

Abstract: A cell expansion technique to amass large numbers of cells from a single specimen for research experiments and clinical trials would greatly benefit the stem cell community. Many current expansion methods are laborious and costly, and those involving ... ...

Abstract	A cell expansion technique to amass large numbers of cells from a single specimen for research experiments and clinical trials would greatly benefit the stem cell community. Many current expansion methods are laborious and costly, and those involving complete dissociation may cause several stem and progenitor cell types to undergo differentiation or early senescence. To overcome these problems, we have developed an automated mechanical passaging method referred to as "chopping" that is simple and inexpensive. This technique avoids chemical or enzymatic dissociation into single cells and instead allows for the large-scale expansion of suspended, spheroid cultures that maintain constant cell/cell contact. The chopping method has primarily been used for fetal brain-derived neural progenitor cells or neurospheres, and has recently been published for use with neural stem cells derived from embryonic and induced pluripotent stem cells. The procedure involves seeding neurospheres onto a tissue culture Petri dish and subsequently passing a sharp, sterile blade through the cells effectively automating the tedious process of manually mechanically dissociating each sphere. Suspending cells in culture provides a favorable surface area-to-volume ratio; as over 500,000 cells can be grown within a single neurosphere of less than 0.5 mm in diameter. In one T175 flask, over 50 million cells can grow in suspension cultures compared to only 15 million in adherent cultures. Importantly, the chopping procedure has been used under current good manufacturing practice (cGMP), permitting mass quantity production of clinical-grade cell products.
MeSH term(s)	Brain/cytology ; Brain/embryology ; Cell Aggregation/physiology ; Cell Communication/physiology ; Cell Growth Processes/physiology ; Cytological Techniques/methods ; Humans ; Neural Stem Cells/cytology ; Pluripotent Stem Cells/cytology
Language	English
Publishing date	2014-06-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Video-Audio Media
ZDB-ID	2259946-0
ISSN	1940-087X ; 1940-087X
ISSN (online)	1940-087X
ISSN	1940-087X
DOI	10.3791/51219
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Article ; Online: Stem cell transplantation for motor neuron disease: current approaches and future perspectives.

Gowing, Genevieve / Svendsen, Clive N

Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics

2011 Volume 8, Issue 4, Page(s) 591–606

Abstract: Motor neuron degeneration leading to muscle atrophy and death is a pathological hallmark of disorders, such as amyotrophic lateral sclerosis or spinal muscular atrophy. No effective treatment is available for these devastating diseases. At present, cell- ... ...

Abstract	Motor neuron degeneration leading to muscle atrophy and death is a pathological hallmark of disorders, such as amyotrophic lateral sclerosis or spinal muscular atrophy. No effective treatment is available for these devastating diseases. At present, cell-based therapies targeting motor neuron replacement, support, or as a vehicle for the delivery of neuroprotective molecules are being investigated. Although many challenges and questions remain, the beneficial effects observed following transplantation therapy in animal models of motor neuron disease has sparked hope and a number of clinical trials. Here, we provide a comprehensive review of cell-based therapeutics for motor neuron disorders, with a particular emphasis on amyotrophic lateral sclerosis.
MeSH term(s)	Animals ; Humans ; Mice ; Motor Neuron Disease/surgery ; Neurons/physiology ; Stem Cell Transplantation/methods ; Stem Cell Transplantation/trends
Language	English
Publishing date	2011-09-06
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2316693-9
ISSN	1878-7479 ; 1933-7213
ISSN (online)	1878-7479
ISSN	1933-7213
DOI	10.1007/s13311-011-0068-7
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Article: A cgmp-applicable expansion method for aggregates of human neural stem and progenitor cells derived from pluripotent stem cells or fetal brain tissue

Shelley, Brandon C / Gowing, Geneviève / Svendsen, Clive N

Journal of visualized experiments. 2014 June 15, , no. 88

2014

Abstract	A cell expansion technique to amass large numbers of cells from a single specimen for research experiments and clinical trials would greatly benefit the stem cell community. Many current expansion methods are laborious and costly, and those involving complete dissociation may cause several stem and progenitor cell types to undergo differentiation or early senescence. To overcome these problems, we have developed an automated mechanical passaging method referred to as “chopping” that is simple and inexpensive. This technique avoids chemical or enzymatic dissociation into single cells and instead allows for the large-scale expansion of suspended, spheroid cultures that maintain constant cell/cell contact. The chopping method has primarily been used for fetal brain-derived neural progenitor cells or neurospheres, and has recently been published for use with neural stem cells derived from embryonic and induced pluripotent stem cells. The procedure involves seeding neurospheres onto a tissue culture Petri dish and subsequently passing a sharp, sterile blade through the cells effectively automating the tedious process of manually mechanically dissociating each sphere. Suspending cells in culture provides a favorable surface area-to-volume ratio; as over 500,000 cells can be grown within a single neurosphere of less than 0.5 mm in diameter. In one T175 flask, over 50 million cells can grow in suspension cultures compared to only 15 million in adherent cultures. Importantly, the chopping procedure has been used under current good manufacturing practice (cGMP), permitting mass quantity production of clinical-grade cell products.
Keywords	automation ; brain ; chopping ; clinical trials ; dissociation ; good manufacturing practices ; neural stem cells ; tissue culture
Language	English
Dates of publication	2014-0615
Size	p. e51219.
Publishing place	Journal of Visualized Experiments
Document type	Article
ZDB-ID	2259946-0
ISSN	1940-087X
ISSN	1940-087X
DOI	10.3791/51219
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Article ; Online: The past, present and future of stem cell clinical trials for ALS.

Thomsen, Gretchen M / Gowing, Genevieve / Svendsen, Soshana / Svendsen, Clive N

Experimental neurology

2014 Volume 262 Pt B, Page(s) 127–137

Abstract: Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disorder that is characterized by progressive degeneration of motor neurons in the cortex, brainstem and spinal cord. This leads to paralysis, respiratory insufficiency and death ... ...

Abstract	Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disorder that is characterized by progressive degeneration of motor neurons in the cortex, brainstem and spinal cord. This leads to paralysis, respiratory insufficiency and death within an average of 3 to 5 years from disease onset. While the genetics of ALS are becoming more understood in familial cases, the mechanisms underlying disease pathology remain unclear and there are no effective treatment options. Without understanding what causes ALS it is difficult to design treatments. However, in recent years stem cell transplantation has emerged as a potential new therapy for ALS patients. While motor neuron replacement remains a focus of some studies trying to treat ALS with stem cells, there is more rationale for using stem cells as support cells for dying motor neurons as they are already connected to the muscle. This could be through reducing inflammation, releasing growth factors, and other potential less understood mechanisms. Prior to moving into patients, stringent pre-clinical studies are required that have at least some rationale and efficacy in animal models and good safety profiles. However, given our poor understanding of what causes ALS and whether stem cells may ameliorate symptoms, there should be a push to determine cell safety in pre-clinical models and then a quick translation to the clinic where patient trials will show if there is any efficacy. Here, we provide a critical review of current clinical trials using either mesenchymal or neural stem cells to treat ALS patients. Pre-clinical data leading to these trials, as well as those in development are also evaluated in terms of mechanisms of action, validity of conclusions and rationale for advancing stem cell treatment strategies for this devastating disorder.
MeSH term(s)	Amyotrophic Lateral Sclerosis/therapy ; Animals ; Clinical Trials as Topic/history ; Clinical Trials as Topic/methods ; Clinical Trials as Topic/trends ; History, 20th Century ; History, 21st Century ; Humans ; Stem Cell Transplantation/methods ; Stem Cell Transplantation/trends
Language	English
Publishing date	2014-12
Publishing country	United States
Document type	Historical Article ; Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	207148-4
ISSN	1090-2430 ; 0014-4886
ISSN (online)	1090-2430
ISSN	0014-4886
DOI	10.1016/j.expneurol.2014.02.021
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Zs.A 184: Show issues

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Article ; Online: Ablation of proliferating cells in the CNS exacerbates motor neuron disease caused by mutant superoxide dismutase.

Audet, Jean-Nicolas / Gowing, Geneviève / Paradis, Renée / Soucy, Geneviève / Julien, Jean-Pierre

PloS one

2012 Volume 7, Issue 4, Page(s) e34932

Abstract: Proliferation of glia and immune cells is a common pathological feature of many neurodegenerative diseases including amyotrophic lateral sclerosis (ALS). Here, to investigate the role of proliferating cells in motor neuron disease, SOD1(G93A) transgenic ... ...

Abstract	Proliferation of glia and immune cells is a common pathological feature of many neurodegenerative diseases including amyotrophic lateral sclerosis (ALS). Here, to investigate the role of proliferating cells in motor neuron disease, SOD1(G93A) transgenic mice were treated intracerebroventicularly (i.c.v.) with the anti-mitotic drug cytosine arabinoside (Ara-C). I.c.v. delivery of Ara-C accelerated disease progression in SOD1(G93A) mouse model of ALS. Ara-C treatment caused substantial decreases in the number of microglia, NG2+ progenitors, Olig2+ cells and CD3+ T cells in the lumbar spinal cord of symptomatic SOD1(G93A) transgenic mice. Exacerbation of disease was also associated with significant alterations in the expression inflammatory molecules IL-1β, IL-6, TGF-β and the growth factor IGF-1.
MeSH term(s)	Amyotrophic Lateral Sclerosis/pathology ; Animals ; Cell Proliferation/drug effects ; Cytarabine/pharmacology ; Disease Models, Animal ; Disease Progression ; Humans ; Insulin-Like Growth Factor I/metabolism ; Interleukin-6/metabolism ; Mice ; Mice, Transgenic ; Microglia/drug effects ; Motor Neuron Disease/complications ; Superoxide Dismutase/genetics ; Transforming Growth Factor beta/metabolism
Chemical Substances	Interleukin-6 ; Transforming Growth Factor beta ; Cytarabine (04079A1RDZ) ; Insulin-Like Growth Factor I (67763-96-6) ; Superoxide Dismutase (EC 1.15.1.1)
Language	English
Publishing date	2012-04-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0034932
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Article ; Online: Ablation of proliferating cells in the CNS exacerbates motor neuron disease caused by mutant superoxide dismutase.

Jean-Nicolas Audet / Geneviève Gowing / Renée Paradis / Geneviève Soucy / Jean-Pierre Julien

PLoS ONE, Vol 7, Iss 4, p e

2012 Volume 34932

Abstract	Proliferation of glia and immune cells is a common pathological feature of many neurodegenerative diseases including amyotrophic lateral sclerosis (ALS). Here, to investigate the role of proliferating cells in motor neuron disease, SOD1(G93A) transgenic mice were treated intracerebroventicularly (i.c.v.) with the anti-mitotic drug cytosine arabinoside (Ara-C). I.c.v. delivery of Ara-C accelerated disease progression in SOD1(G93A) mouse model of ALS. Ara-C treatment caused substantial decreases in the number of microglia, NG2+ progenitors, Olig2+ cells and CD3+ T cells in the lumbar spinal cord of symptomatic SOD1(G93A) transgenic mice. Exacerbation of disease was also associated with significant alterations in the expression inflammatory molecules IL-1β, IL-6, TGF-β and the growth factor IGF-1.
Keywords	Medicine ; R ; Science ; Q
Language	English
Publishing date	2012-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
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Article ; Online: Wild-type human SOD1 overexpression does not accelerate motor neuron disease in mice expressing murine Sod1 G86R.

Audet, Jean-Nicolas / Gowing, Geneviève / Julien, Jean-Pierre

Neurobiology of disease

2010 Volume 40, Issue 1, Page(s) 245–250

Abstract: Approximately 10% of the cases of amyotrophic lateral sclerosis (ALS) are inherited, with the majority of identified linkages in the gene encoding Cu/Zn superoxide dismutase (SOD1). Recent studies showed that human wild-type SOD1 (SOD1(WT)) ... ...

Abstract	Approximately 10% of the cases of amyotrophic lateral sclerosis (ALS) are inherited, with the majority of identified linkages in the gene encoding Cu/Zn superoxide dismutase (SOD1). Recent studies showed that human wild-type SOD1 (SOD1(WT)) overexpression accelerated disease in mice expressing human SOD1 mutants linked to ALS. However, there is a controversy whether the exacerbation mechanism occurs through coaggregation of human SOD1(WT) with SOD1 mutants, stabilization by SOD1(WT) of toxic soluble SOD1 species, or conversion of SOD1(WT) into toxic species through oxidative damage. To further address whether the exacerbation of disease requires misfolding, modifications, and/or interaction of SOD1(WT) with pathogenic forms of SOD1 species, we have studied the effect of human SOD1(WT) overexpression in mice expressing the murine mutant Sod1(G86R). Surprisingly, unlike a previous report with SOD1(G85R) mice, SOD1(WT) overexpression did not affect the life span of Sod1(G86R) mice. Our analysis of spinal cord extracts revealed a lack of heterodimerization or aggregation between human SOD1(WT) and mouse Sod1(G86R) proteins. Moreover, there was no evidence of conversion of SOD1(WT) into misfolded or abnormal SOD1 isoforms based on immunoreactivity with monoclonal antibodies specific to misfolded forms of SOD1 mutants and on analysis of SOD1 isoforms after two-dimensional gel electrophoresis. We conclude that a direct interaction between wild type and mutant forms of SOD1 is required for exacerbation of ALS disease by SOD1(WT) protein.
MeSH term(s)	Amino Acid Sequence ; Animals ; Base Sequence ; Disease Models, Animal ; Disease Progression ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Molecular Sequence Data ; Motor Neuron Disease/enzymology ; Motor Neuron Disease/genetics ; Motor Neuron Disease/pathology ; Mutation ; Spinal Cord/enzymology ; Spinal Cord/pathology ; Superoxide Dismutase/biosynthesis ; Superoxide Dismutase/genetics ; Superoxide Dismutase/physiology ; Superoxide Dismutase-1
Chemical Substances	SOD1 protein, human ; Sod1 protein, mouse (EC 1.15.1.1) ; Superoxide Dismutase (EC 1.15.1.1) ; Superoxide Dismutase-1 (EC 1.15.1.1)
Language	English
Publishing date	2010-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2010.05.031
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Zs.A 4444: Show issues

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Article ; Online: Transplantation of human neural progenitor cells secreting GDNF into the spinal cord of patients with ALS: a phase 1/2a trial.

Baloh, Robert H / Johnson, J Patrick / Avalos, Pablo / Allred, Peggy / Svendsen, Soshana / Gowing, Genevieve / Roxas, Kristina / Wu, Amanda / Donahue, Becky / Osborne, Sheryl / Lawless, George / Shelley, Brandon / Wheeler, Koral / Prina, Carolyn / Fine, Dana / Kendra-Romito, Tami / Stokes, Haniah / Manoukian, Vicki / Muthukumaran, Abirami /

Garcia, Leslie / Bañuelos, Maria G / Godoy, Marlesa / Bresee, Catherine / Yu, Hong / Drazin, Doniel / Ross, Lindsey / Naruse, Robert / Babu, Harish / Macklin, Eric A / Vo, Ashley / Elsayegh, Ashraf / Tourtellotte, Warren / Maya, Marcel / Burford, Matthew / Diaz, Frank / Patil, Chirag G / Lewis, Richard A / Svendsen, Clive N

Nature medicine

2022 Volume 28, Issue 9, Page(s) 1813–1822

Abstract: Amyotrophic lateral sclerosis (ALS) involves progressive motor neuron loss, leading to paralysis and death typically within 3-5 years of diagnosis. Dysfunctional astrocytes may contribute to disease and glial cell line-derived neurotrophic factor (GDNF) ... ...

Abstract	Amyotrophic lateral sclerosis (ALS) involves progressive motor neuron loss, leading to paralysis and death typically within 3-5 years of diagnosis. Dysfunctional astrocytes may contribute to disease and glial cell line-derived neurotrophic factor (GDNF) can be protective. Here we show that human neural progenitor cells transduced with GDNF (CNS10-NPC-GDNF) differentiated to astrocytes protected spinal motor neurons and were safe in animal models. CNS10-NPC-GDNF were transplanted unilaterally into the lumbar spinal cord of 18 ALS participants in a phase 1/2a study (NCT02943850). The primary endpoint of safety at 1 year was met, with no negative effect of the transplant on motor function in the treated leg compared with the untreated leg. Tissue analysis of 13 participants who died of disease progression showed graft survival and GDNF production. Benign neuromas near delivery sites were common incidental findings at post-mortem. This study shows that one administration of engineered neural progenitors can provide new support cells and GDNF delivery to the ALS patient spinal cord for up to 42 months post-transplantation.
MeSH term(s)	Amyotrophic Lateral Sclerosis/therapy ; Animals ; Disease Models, Animal ; Glial Cell Line-Derived Neurotrophic Factor/genetics ; Humans ; Neural Stem Cells ; Spinal Cord ; Superoxide Dismutase
Chemical Substances	Glial Cell Line-Derived Neurotrophic Factor ; Superoxide Dismutase (EC 1.15.1.1)
Language	English
Publishing date	2022-09-05
Publishing country	United States
Document type	Clinical Trial, Phase I ; Clinical Trial, Phase II ; Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1220066-9
ISSN	1546-170X ; 1078-8956
ISSN (online)	1546-170X
ISSN	1078-8956
DOI	10.1038/s41591-022-01956-3
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Zs.A 4212: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Absence of tumor necrosis factor-alpha does not affect motor neuron disease caused by superoxide dismutase 1 mutations.

Gowing, Geneviève / Dequen, Florence / Soucy, Geneviève / Julien, Jean-Pierre

The Journal of neuroscience : the official journal of the Society for Neuroscience

2006 Volume 26, Issue 44, Page(s) 11397–11402

Abstract: An increase in the expression of the proinflammatory cytokine tumor necrosis factor alpha (TNF-alpha) has been observed in patients with amyotrophic lateral sclerosis (ALS) and in the mice models of the disease. TNF-alpha is a potent activator of ... ...

Abstract	An increase in the expression of the proinflammatory cytokine tumor necrosis factor alpha (TNF-alpha) has been observed in patients with amyotrophic lateral sclerosis (ALS) and in the mice models of the disease. TNF-alpha is a potent activator of macrophages and microglia and, under certain conditions, can induce or exacerbate neuronal cell death. Here, we assessed the contribution of TNF-alpha in motor neuron disease in mice overexpressing mutant superoxide dismutase 1 (SOD1) genes linked to familial ALS. This was accomplished by the generation of mice expressing SOD1(G37R) or SOD1(G93A) mutants in the context of TNF-alpha gene knock out. Surprisingly, the absence of TNF-alpha did not affect the lifespan or the extent of motor neuron loss in SOD1 transgenic mice. These results provide compelling evidence indicating that TNF-alpha does not directly contribute to motor neuron degeneration caused by SOD1 mutations.
MeSH term(s)	Animals ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Motor Neuron Disease/enzymology ; Motor Neuron Disease/genetics ; Motor Neuron Disease/pathology ; Mutation ; Superoxide Dismutase/genetics ; Superoxide Dismutase/metabolism ; Superoxide Dismutase-1 ; Tumor Necrosis Factor-alpha/deficiency ; Tumor Necrosis Factor-alpha/genetics ; Tumor Necrosis Factor-alpha/physiology
Chemical Substances	Tumor Necrosis Factor-alpha ; Sod1 protein, mouse (EC 1.15.1.1) ; Superoxide Dismutase (EC 1.15.1.1) ; Superoxide Dismutase-1 (EC 1.15.1.1)
Language	English
Publishing date	2006-02-17
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604637-x
ISSN	1529-2401 ; 0270-6474
ISSN (online)	1529-2401
ISSN	0270-6474
DOI	10.1523/JNEUROSCI.0602-06.2006
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