Differential expression of inflammation- and apoptosis-related genes in spinal cords of a mutant SOD1 transgenic mouse model of familial amyotrophic lateral sclerosis
Familial amyotrophic lateral sclerosis (FALS)-linked mutations in copper–zinc superoxide dismutase (SOD1) cause motor neuron death through one or more acquired toxic properties. We analyzed the molecular mechanism underlying motor neuron degeneration in the transgenic mouse model expressing the SOD1...
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| Autor*in: |
Yoshihara, Tsuyoshi [verfasserIn] Ishigaki, Shinsuke [verfasserIn] Yamamoto, Masahiko [verfasserIn] |
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E-Artikel |
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| Erschienen: |
Oxford, UK: Blackwell Science, Ltd ; 2002 |
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Online-Ressource |
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| Reproduktion: |
2001 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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In: Journal of neurochemistry - Oxford : Wiley-Blackwell, 1956, 80(2002), 1, Seite 0 |
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volume:80 ; year:2002 ; number:1 ; pages:0 |
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| DOI / URN: |
10.1046/j.0022-3042.2001.00683.x |
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| 520 | |a Familial amyotrophic lateral sclerosis (FALS)-linked mutations in copper–zinc superoxide dismutase (SOD1) cause motor neuron death through one or more acquired toxic properties. We analyzed the molecular mechanism underlying motor neuron degeneration in the transgenic mouse model expressing the SOD1 gene with G93A mutation. Using cDNA microarray, the differentially expressed genes were identified in the spinal cords of G93A mice, 30 being elevated and seven decreased. cDNA microarray analysis to monitor gene expression during neurodegeneration revealed an up-regulation of genes related to an inflammatory process, such as the tumor necrosis factor-α (TNF-α) gene, resulting from glial cell activation, together with the change in apoptosis-related gene expression, such as caspase-1. The increased expression of the inflammation- and apoptosis-related genes occurred at 11 weeks of age in the presymptomatic stage prior to motor neuron death. These results suggest a mechanism of neurodegeneration that includes an inflammatory response as an important component. Thus, ALS has paralleled other neurodegenerative disorders, such as Alzheimer's and prion diseases, in which the inflammatory process is believed to participate directly in neuronal death. | ||
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10.1046/j.0022-3042.2001.00683.x doi (DE-627)NLEJ243139861 DE-627 ger DE-627 rakwb Yoshihara, Tsuyoshi verfasserin aut Differential expression of inflammation- and apoptosis-related genes in spinal cords of a mutant SOD1 transgenic mouse
model of familial amyotrophic lateral sclerosis Oxford, UK Blackwell Science, Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Familial amyotrophic lateral sclerosis (FALS)-linked mutations in copper–zinc superoxide dismutase (SOD1) cause motor neuron death through one or more acquired toxic properties. We analyzed the molecular mechanism underlying motor neuron degeneration in the transgenic mouse model expressing the SOD1 gene with G93A mutation. Using cDNA microarray, the differentially expressed genes were identified in the spinal cords of G93A mice, 30 being elevated and seven decreased. cDNA microarray analysis to monitor gene expression during neurodegeneration revealed an up-regulation of genes related to an inflammatory process, such as the tumor necrosis factor-α (TNF-α) gene, resulting from glial cell activation, together with the change in apoptosis-related gene expression, such as caspase-1. The increased expression of the inflammation- and apoptosis-related genes occurred at 11 weeks of age in the presymptomatic stage prior to motor neuron death. These results suggest a mechanism of neurodegeneration that includes an inflammatory response as an important component. Thus, ALS has paralleled other neurodegenerative disorders, such as Alzheimer's and prion diseases, in which the inflammatory process is believed to participate directly in neuronal death. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| amyotrophic lateral sclerosis (ALS) Ishigaki, Shinsuke verfasserin aut Yamamoto, Masahiko verfasserin aut Liang, Yideng oth Niwa, Ichi oth Takeuchi, Hideyuki oth Doyu, Manabu oth Sobue, Gen oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 80(2002), 1, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:80 year:2002 number:1 pages:0 http://dx.doi.org/10.1046/j.0022-3042.2001.00683.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 80 2002 1 0 |
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10.1046/j.0022-3042.2001.00683.x doi (DE-627)NLEJ243139861 DE-627 ger DE-627 rakwb Yoshihara, Tsuyoshi verfasserin aut Differential expression of inflammation- and apoptosis-related genes in spinal cords of a mutant SOD1 transgenic mouse
model of familial amyotrophic lateral sclerosis Oxford, UK Blackwell Science, Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Familial amyotrophic lateral sclerosis (FALS)-linked mutations in copper–zinc superoxide dismutase (SOD1) cause motor neuron death through one or more acquired toxic properties. We analyzed the molecular mechanism underlying motor neuron degeneration in the transgenic mouse model expressing the SOD1 gene with G93A mutation. Using cDNA microarray, the differentially expressed genes were identified in the spinal cords of G93A mice, 30 being elevated and seven decreased. cDNA microarray analysis to monitor gene expression during neurodegeneration revealed an up-regulation of genes related to an inflammatory process, such as the tumor necrosis factor-α (TNF-α) gene, resulting from glial cell activation, together with the change in apoptosis-related gene expression, such as caspase-1. The increased expression of the inflammation- and apoptosis-related genes occurred at 11 weeks of age in the presymptomatic stage prior to motor neuron death. These results suggest a mechanism of neurodegeneration that includes an inflammatory response as an important component. Thus, ALS has paralleled other neurodegenerative disorders, such as Alzheimer's and prion diseases, in which the inflammatory process is believed to participate directly in neuronal death. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| amyotrophic lateral sclerosis (ALS) Ishigaki, Shinsuke verfasserin aut Yamamoto, Masahiko verfasserin aut Liang, Yideng oth Niwa, Ichi oth Takeuchi, Hideyuki oth Doyu, Manabu oth Sobue, Gen oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 80(2002), 1, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:80 year:2002 number:1 pages:0 http://dx.doi.org/10.1046/j.0022-3042.2001.00683.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 80 2002 1 0 |
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10.1046/j.0022-3042.2001.00683.x doi (DE-627)NLEJ243139861 DE-627 ger DE-627 rakwb Yoshihara, Tsuyoshi verfasserin aut Differential expression of inflammation- and apoptosis-related genes in spinal cords of a mutant SOD1 transgenic mouse
model of familial amyotrophic lateral sclerosis Oxford, UK Blackwell Science, Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Familial amyotrophic lateral sclerosis (FALS)-linked mutations in copper–zinc superoxide dismutase (SOD1) cause motor neuron death through one or more acquired toxic properties. We analyzed the molecular mechanism underlying motor neuron degeneration in the transgenic mouse model expressing the SOD1 gene with G93A mutation. Using cDNA microarray, the differentially expressed genes were identified in the spinal cords of G93A mice, 30 being elevated and seven decreased. cDNA microarray analysis to monitor gene expression during neurodegeneration revealed an up-regulation of genes related to an inflammatory process, such as the tumor necrosis factor-α (TNF-α) gene, resulting from glial cell activation, together with the change in apoptosis-related gene expression, such as caspase-1. The increased expression of the inflammation- and apoptosis-related genes occurred at 11 weeks of age in the presymptomatic stage prior to motor neuron death. These results suggest a mechanism of neurodegeneration that includes an inflammatory response as an important component. Thus, ALS has paralleled other neurodegenerative disorders, such as Alzheimer's and prion diseases, in which the inflammatory process is believed to participate directly in neuronal death. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| amyotrophic lateral sclerosis (ALS) Ishigaki, Shinsuke verfasserin aut Yamamoto, Masahiko verfasserin aut Liang, Yideng oth Niwa, Ichi oth Takeuchi, Hideyuki oth Doyu, Manabu oth Sobue, Gen oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 80(2002), 1, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:80 year:2002 number:1 pages:0 http://dx.doi.org/10.1046/j.0022-3042.2001.00683.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 80 2002 1 0 |
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10.1046/j.0022-3042.2001.00683.x doi (DE-627)NLEJ243139861 DE-627 ger DE-627 rakwb Yoshihara, Tsuyoshi verfasserin aut Differential expression of inflammation- and apoptosis-related genes in spinal cords of a mutant SOD1 transgenic mouse
model of familial amyotrophic lateral sclerosis Oxford, UK Blackwell Science, Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Familial amyotrophic lateral sclerosis (FALS)-linked mutations in copper–zinc superoxide dismutase (SOD1) cause motor neuron death through one or more acquired toxic properties. We analyzed the molecular mechanism underlying motor neuron degeneration in the transgenic mouse model expressing the SOD1 gene with G93A mutation. Using cDNA microarray, the differentially expressed genes were identified in the spinal cords of G93A mice, 30 being elevated and seven decreased. cDNA microarray analysis to monitor gene expression during neurodegeneration revealed an up-regulation of genes related to an inflammatory process, such as the tumor necrosis factor-α (TNF-α) gene, resulting from glial cell activation, together with the change in apoptosis-related gene expression, such as caspase-1. The increased expression of the inflammation- and apoptosis-related genes occurred at 11 weeks of age in the presymptomatic stage prior to motor neuron death. These results suggest a mechanism of neurodegeneration that includes an inflammatory response as an important component. Thus, ALS has paralleled other neurodegenerative disorders, such as Alzheimer's and prion diseases, in which the inflammatory process is believed to participate directly in neuronal death. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| amyotrophic lateral sclerosis (ALS) Ishigaki, Shinsuke verfasserin aut Yamamoto, Masahiko verfasserin aut Liang, Yideng oth Niwa, Ichi oth Takeuchi, Hideyuki oth Doyu, Manabu oth Sobue, Gen oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 80(2002), 1, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:80 year:2002 number:1 pages:0 http://dx.doi.org/10.1046/j.0022-3042.2001.00683.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 80 2002 1 0 |
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10.1046/j.0022-3042.2001.00683.x doi (DE-627)NLEJ243139861 DE-627 ger DE-627 rakwb Yoshihara, Tsuyoshi verfasserin aut Differential expression of inflammation- and apoptosis-related genes in spinal cords of a mutant SOD1 transgenic mouse
model of familial amyotrophic lateral sclerosis Oxford, UK Blackwell Science, Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Familial amyotrophic lateral sclerosis (FALS)-linked mutations in copper–zinc superoxide dismutase (SOD1) cause motor neuron death through one or more acquired toxic properties. We analyzed the molecular mechanism underlying motor neuron degeneration in the transgenic mouse model expressing the SOD1 gene with G93A mutation. Using cDNA microarray, the differentially expressed genes were identified in the spinal cords of G93A mice, 30 being elevated and seven decreased. cDNA microarray analysis to monitor gene expression during neurodegeneration revealed an up-regulation of genes related to an inflammatory process, such as the tumor necrosis factor-α (TNF-α) gene, resulting from glial cell activation, together with the change in apoptosis-related gene expression, such as caspase-1. The increased expression of the inflammation- and apoptosis-related genes occurred at 11 weeks of age in the presymptomatic stage prior to motor neuron death. These results suggest a mechanism of neurodegeneration that includes an inflammatory response as an important component. Thus, ALS has paralleled other neurodegenerative disorders, such as Alzheimer's and prion diseases, in which the inflammatory process is believed to participate directly in neuronal death. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| amyotrophic lateral sclerosis (ALS) Ishigaki, Shinsuke verfasserin aut Yamamoto, Masahiko verfasserin aut Liang, Yideng oth Niwa, Ichi oth Takeuchi, Hideyuki oth Doyu, Manabu oth Sobue, Gen oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 80(2002), 1, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:80 year:2002 number:1 pages:0 http://dx.doi.org/10.1046/j.0022-3042.2001.00683.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 80 2002 1 0 |
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Differential expression of inflammation- and apoptosis-related genes in spinal cords of a mutant SOD1 transgenic mouse
model of familial amyotrophic lateral sclerosis |
| abstract |
Familial amyotrophic lateral sclerosis (FALS)-linked mutations in copper–zinc superoxide dismutase (SOD1) cause motor neuron death through one or more acquired toxic properties. We analyzed the molecular mechanism underlying motor neuron degeneration in the transgenic mouse model expressing the SOD1 gene with G93A mutation. Using cDNA microarray, the differentially expressed genes were identified in the spinal cords of G93A mice, 30 being elevated and seven decreased. cDNA microarray analysis to monitor gene expression during neurodegeneration revealed an up-regulation of genes related to an inflammatory process, such as the tumor necrosis factor-α (TNF-α) gene, resulting from glial cell activation, together with the change in apoptosis-related gene expression, such as caspase-1. The increased expression of the inflammation- and apoptosis-related genes occurred at 11 weeks of age in the presymptomatic stage prior to motor neuron death. These results suggest a mechanism of neurodegeneration that includes an inflammatory response as an important component. Thus, ALS has paralleled other neurodegenerative disorders, such as Alzheimer's and prion diseases, in which the inflammatory process is believed to participate directly in neuronal death. |
| abstractGer |
Familial amyotrophic lateral sclerosis (FALS)-linked mutations in copper–zinc superoxide dismutase (SOD1) cause motor neuron death through one or more acquired toxic properties. We analyzed the molecular mechanism underlying motor neuron degeneration in the transgenic mouse model expressing the SOD1 gene with G93A mutation. Using cDNA microarray, the differentially expressed genes were identified in the spinal cords of G93A mice, 30 being elevated and seven decreased. cDNA microarray analysis to monitor gene expression during neurodegeneration revealed an up-regulation of genes related to an inflammatory process, such as the tumor necrosis factor-α (TNF-α) gene, resulting from glial cell activation, together with the change in apoptosis-related gene expression, such as caspase-1. The increased expression of the inflammation- and apoptosis-related genes occurred at 11 weeks of age in the presymptomatic stage prior to motor neuron death. These results suggest a mechanism of neurodegeneration that includes an inflammatory response as an important component. Thus, ALS has paralleled other neurodegenerative disorders, such as Alzheimer's and prion diseases, in which the inflammatory process is believed to participate directly in neuronal death. |
| abstract_unstemmed |
Familial amyotrophic lateral sclerosis (FALS)-linked mutations in copper–zinc superoxide dismutase (SOD1) cause motor neuron death through one or more acquired toxic properties. We analyzed the molecular mechanism underlying motor neuron degeneration in the transgenic mouse model expressing the SOD1 gene with G93A mutation. Using cDNA microarray, the differentially expressed genes were identified in the spinal cords of G93A mice, 30 being elevated and seven decreased. cDNA microarray analysis to monitor gene expression during neurodegeneration revealed an up-regulation of genes related to an inflammatory process, such as the tumor necrosis factor-α (TNF-α) gene, resulting from glial cell activation, together with the change in apoptosis-related gene expression, such as caspase-1. The increased expression of the inflammation- and apoptosis-related genes occurred at 11 weeks of age in the presymptomatic stage prior to motor neuron death. These results suggest a mechanism of neurodegeneration that includes an inflammatory response as an important component. Thus, ALS has paralleled other neurodegenerative disorders, such as Alzheimer's and prion diseases, in which the inflammatory process is believed to participate directly in neuronal death. |
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Differential expression of inflammation- and apoptosis-related genes in spinal cords of a mutant SOD1 transgenic mouse
model of familial amyotrophic lateral sclerosis |
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Ishigaki, Shinsuke Yamamoto, Masahiko Liang, Yideng Niwa, Ichi Takeuchi, Hideyuki Doyu, Manabu Sobue, Gen |
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Ishigaki, Shinsuke Yamamoto, Masahiko Liang, Yideng Niwa, Ichi Takeuchi, Hideyuki Doyu, Manabu Sobue, Gen |
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