Gene therapy for epilepsy
Gene therapy may represent an effective alternative to standard pharmacological approaches for certain forms of epilepsy. Currently, the best candidates for this therapeutic approach appear to be epilepsies characterized by a focal lesion. Gene therapy has been attempted to produce antiepileptogenic...
Ausführliche Beschreibung
Autor*in: |
Simonato, Michele [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2014transfer abstract |
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Umfang: |
6 |
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Übergeordnetes Werk: |
Enthalten in: Effect of morphology and molecular orientation on environmental water biodegradability of poly[( - Komiyama, Katsuya ELSEVIER, 2021, New York, NY [u.a.] |
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Übergeordnetes Werk: |
volume:38 ; year:2014 ; pages:125-130 ; extent:6 |
Links: |
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DOI / URN: |
10.1016/j.yebeh.2013.09.013 |
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Katalog-ID: |
ELV017332699 |
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520 | |a Gene therapy may represent an effective alternative to standard pharmacological approaches for certain forms of epilepsy. Currently, the best candidates for this therapeutic approach appear to be epilepsies characterized by a focal lesion. Gene therapy has been attempted to produce antiepileptogenic (prevention of development of epilepsy in subject at risk after having received an epileptogenic insult), antiseizure (reduction of frequency and/or severity of seizures), and disease-modifying (alteration of the natural history of the disease) effects. An example of gene therapy aimed at producing antiepileptogenic effects is a combination therapy based on the supplementation of the neurotrophic factors brain-derived neurotrophic factor (BDNF) and fibroblast growth factor 2 (FGF-2). Antiseizure effects have been obtained by increasing the strength of inhibitory signals (by supplementing specific GABAA receptor subunits or inhibitory neuropeptides like galanin or neuropeptide Y) or by reducing the strength of excitatory signals (by knocking down NMDA receptor subunits). This review summarizes the results obtained to date using gene therapy in epilepsy models and discusses the challenges and the opportunities that this approach can offer for the treatment of human epilepsies. | ||
520 | |a Gene therapy may represent an effective alternative to standard pharmacological approaches for certain forms of epilepsy. Currently, the best candidates for this therapeutic approach appear to be epilepsies characterized by a focal lesion. Gene therapy has been attempted to produce antiepileptogenic (prevention of development of epilepsy in subject at risk after having received an epileptogenic insult), antiseizure (reduction of frequency and/or severity of seizures), and disease-modifying (alteration of the natural history of the disease) effects. An example of gene therapy aimed at producing antiepileptogenic effects is a combination therapy based on the supplementation of the neurotrophic factors brain-derived neurotrophic factor (BDNF) and fibroblast growth factor 2 (FGF-2). Antiseizure effects have been obtained by increasing the strength of inhibitory signals (by supplementing specific GABAA receptor subunits or inhibitory neuropeptides like galanin or neuropeptide Y) or by reducing the strength of excitatory signals (by knocking down NMDA receptor subunits). This review summarizes the results obtained to date using gene therapy in epilepsy models and discusses the challenges and the opportunities that this approach can offer for the treatment of human epilepsies. | ||
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10.1016/j.yebeh.2013.09.013 doi GBVA2014005000004.pica (DE-627)ELV017332699 (ELSEVIER)S1525-5050(13)00479-4 DE-627 ger DE-627 rakwb eng 610 610 DE-600 540 660 VZ 51.70 bkl 35.80 bkl Simonato, Michele verfasserin aut Gene therapy for epilepsy 2014transfer abstract 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Gene therapy may represent an effective alternative to standard pharmacological approaches for certain forms of epilepsy. Currently, the best candidates for this therapeutic approach appear to be epilepsies characterized by a focal lesion. Gene therapy has been attempted to produce antiepileptogenic (prevention of development of epilepsy in subject at risk after having received an epileptogenic insult), antiseizure (reduction of frequency and/or severity of seizures), and disease-modifying (alteration of the natural history of the disease) effects. An example of gene therapy aimed at producing antiepileptogenic effects is a combination therapy based on the supplementation of the neurotrophic factors brain-derived neurotrophic factor (BDNF) and fibroblast growth factor 2 (FGF-2). Antiseizure effects have been obtained by increasing the strength of inhibitory signals (by supplementing specific GABAA receptor subunits or inhibitory neuropeptides like galanin or neuropeptide Y) or by reducing the strength of excitatory signals (by knocking down NMDA receptor subunits). This review summarizes the results obtained to date using gene therapy in epilepsy models and discusses the challenges and the opportunities that this approach can offer for the treatment of human epilepsies. Gene therapy may represent an effective alternative to standard pharmacological approaches for certain forms of epilepsy. Currently, the best candidates for this therapeutic approach appear to be epilepsies characterized by a focal lesion. Gene therapy has been attempted to produce antiepileptogenic (prevention of development of epilepsy in subject at risk after having received an epileptogenic insult), antiseizure (reduction of frequency and/or severity of seizures), and disease-modifying (alteration of the natural history of the disease) effects. An example of gene therapy aimed at producing antiepileptogenic effects is a combination therapy based on the supplementation of the neurotrophic factors brain-derived neurotrophic factor (BDNF) and fibroblast growth factor 2 (FGF-2). Antiseizure effects have been obtained by increasing the strength of inhibitory signals (by supplementing specific GABAA receptor subunits or inhibitory neuropeptides like galanin or neuropeptide Y) or by reducing the strength of excitatory signals (by knocking down NMDA receptor subunits). This review summarizes the results obtained to date using gene therapy in epilepsy models and discusses the challenges and the opportunities that this approach can offer for the treatment of human epilepsies. Enthalten in Elsevier Komiyama, Katsuya ELSEVIER Effect of morphology and molecular orientation on environmental water biodegradability of poly[( 2021 New York, NY [u.a.] (DE-627)ELV006838707 volume:38 year:2014 pages:125-130 extent:6 https://doi.org/10.1016/j.yebeh.2013.09.013 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 51.70 Polymerwerkstoffe Kunststoffe Werkstoffkunde VZ 35.80 Makromolekulare Chemie VZ AR 38 2014 125-130 6 045F 610 |
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10.1016/j.yebeh.2013.09.013 doi GBVA2014005000004.pica (DE-627)ELV017332699 (ELSEVIER)S1525-5050(13)00479-4 DE-627 ger DE-627 rakwb eng 610 610 DE-600 540 660 VZ 51.70 bkl 35.80 bkl Simonato, Michele verfasserin aut Gene therapy for epilepsy 2014transfer abstract 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Gene therapy may represent an effective alternative to standard pharmacological approaches for certain forms of epilepsy. Currently, the best candidates for this therapeutic approach appear to be epilepsies characterized by a focal lesion. Gene therapy has been attempted to produce antiepileptogenic (prevention of development of epilepsy in subject at risk after having received an epileptogenic insult), antiseizure (reduction of frequency and/or severity of seizures), and disease-modifying (alteration of the natural history of the disease) effects. An example of gene therapy aimed at producing antiepileptogenic effects is a combination therapy based on the supplementation of the neurotrophic factors brain-derived neurotrophic factor (BDNF) and fibroblast growth factor 2 (FGF-2). Antiseizure effects have been obtained by increasing the strength of inhibitory signals (by supplementing specific GABAA receptor subunits or inhibitory neuropeptides like galanin or neuropeptide Y) or by reducing the strength of excitatory signals (by knocking down NMDA receptor subunits). This review summarizes the results obtained to date using gene therapy in epilepsy models and discusses the challenges and the opportunities that this approach can offer for the treatment of human epilepsies. Gene therapy may represent an effective alternative to standard pharmacological approaches for certain forms of epilepsy. Currently, the best candidates for this therapeutic approach appear to be epilepsies characterized by a focal lesion. Gene therapy has been attempted to produce antiepileptogenic (prevention of development of epilepsy in subject at risk after having received an epileptogenic insult), antiseizure (reduction of frequency and/or severity of seizures), and disease-modifying (alteration of the natural history of the disease) effects. An example of gene therapy aimed at producing antiepileptogenic effects is a combination therapy based on the supplementation of the neurotrophic factors brain-derived neurotrophic factor (BDNF) and fibroblast growth factor 2 (FGF-2). Antiseizure effects have been obtained by increasing the strength of inhibitory signals (by supplementing specific GABAA receptor subunits or inhibitory neuropeptides like galanin or neuropeptide Y) or by reducing the strength of excitatory signals (by knocking down NMDA receptor subunits). This review summarizes the results obtained to date using gene therapy in epilepsy models and discusses the challenges and the opportunities that this approach can offer for the treatment of human epilepsies. Enthalten in Elsevier Komiyama, Katsuya ELSEVIER Effect of morphology and molecular orientation on environmental water biodegradability of poly[( 2021 New York, NY [u.a.] (DE-627)ELV006838707 volume:38 year:2014 pages:125-130 extent:6 https://doi.org/10.1016/j.yebeh.2013.09.013 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 51.70 Polymerwerkstoffe Kunststoffe Werkstoffkunde VZ 35.80 Makromolekulare Chemie VZ AR 38 2014 125-130 6 045F 610 |
allfields_unstemmed |
10.1016/j.yebeh.2013.09.013 doi GBVA2014005000004.pica (DE-627)ELV017332699 (ELSEVIER)S1525-5050(13)00479-4 DE-627 ger DE-627 rakwb eng 610 610 DE-600 540 660 VZ 51.70 bkl 35.80 bkl Simonato, Michele verfasserin aut Gene therapy for epilepsy 2014transfer abstract 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Gene therapy may represent an effective alternative to standard pharmacological approaches for certain forms of epilepsy. Currently, the best candidates for this therapeutic approach appear to be epilepsies characterized by a focal lesion. Gene therapy has been attempted to produce antiepileptogenic (prevention of development of epilepsy in subject at risk after having received an epileptogenic insult), antiseizure (reduction of frequency and/or severity of seizures), and disease-modifying (alteration of the natural history of the disease) effects. An example of gene therapy aimed at producing antiepileptogenic effects is a combination therapy based on the supplementation of the neurotrophic factors brain-derived neurotrophic factor (BDNF) and fibroblast growth factor 2 (FGF-2). Antiseizure effects have been obtained by increasing the strength of inhibitory signals (by supplementing specific GABAA receptor subunits or inhibitory neuropeptides like galanin or neuropeptide Y) or by reducing the strength of excitatory signals (by knocking down NMDA receptor subunits). This review summarizes the results obtained to date using gene therapy in epilepsy models and discusses the challenges and the opportunities that this approach can offer for the treatment of human epilepsies. Gene therapy may represent an effective alternative to standard pharmacological approaches for certain forms of epilepsy. Currently, the best candidates for this therapeutic approach appear to be epilepsies characterized by a focal lesion. Gene therapy has been attempted to produce antiepileptogenic (prevention of development of epilepsy in subject at risk after having received an epileptogenic insult), antiseizure (reduction of frequency and/or severity of seizures), and disease-modifying (alteration of the natural history of the disease) effects. An example of gene therapy aimed at producing antiepileptogenic effects is a combination therapy based on the supplementation of the neurotrophic factors brain-derived neurotrophic factor (BDNF) and fibroblast growth factor 2 (FGF-2). Antiseizure effects have been obtained by increasing the strength of inhibitory signals (by supplementing specific GABAA receptor subunits or inhibitory neuropeptides like galanin or neuropeptide Y) or by reducing the strength of excitatory signals (by knocking down NMDA receptor subunits). This review summarizes the results obtained to date using gene therapy in epilepsy models and discusses the challenges and the opportunities that this approach can offer for the treatment of human epilepsies. Enthalten in Elsevier Komiyama, Katsuya ELSEVIER Effect of morphology and molecular orientation on environmental water biodegradability of poly[( 2021 New York, NY [u.a.] (DE-627)ELV006838707 volume:38 year:2014 pages:125-130 extent:6 https://doi.org/10.1016/j.yebeh.2013.09.013 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 51.70 Polymerwerkstoffe Kunststoffe Werkstoffkunde VZ 35.80 Makromolekulare Chemie VZ AR 38 2014 125-130 6 045F 610 |
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10.1016/j.yebeh.2013.09.013 doi GBVA2014005000004.pica (DE-627)ELV017332699 (ELSEVIER)S1525-5050(13)00479-4 DE-627 ger DE-627 rakwb eng 610 610 DE-600 540 660 VZ 51.70 bkl 35.80 bkl Simonato, Michele verfasserin aut Gene therapy for epilepsy 2014transfer abstract 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Gene therapy may represent an effective alternative to standard pharmacological approaches for certain forms of epilepsy. Currently, the best candidates for this therapeutic approach appear to be epilepsies characterized by a focal lesion. Gene therapy has been attempted to produce antiepileptogenic (prevention of development of epilepsy in subject at risk after having received an epileptogenic insult), antiseizure (reduction of frequency and/or severity of seizures), and disease-modifying (alteration of the natural history of the disease) effects. An example of gene therapy aimed at producing antiepileptogenic effects is a combination therapy based on the supplementation of the neurotrophic factors brain-derived neurotrophic factor (BDNF) and fibroblast growth factor 2 (FGF-2). Antiseizure effects have been obtained by increasing the strength of inhibitory signals (by supplementing specific GABAA receptor subunits or inhibitory neuropeptides like galanin or neuropeptide Y) or by reducing the strength of excitatory signals (by knocking down NMDA receptor subunits). This review summarizes the results obtained to date using gene therapy in epilepsy models and discusses the challenges and the opportunities that this approach can offer for the treatment of human epilepsies. Gene therapy may represent an effective alternative to standard pharmacological approaches for certain forms of epilepsy. Currently, the best candidates for this therapeutic approach appear to be epilepsies characterized by a focal lesion. Gene therapy has been attempted to produce antiepileptogenic (prevention of development of epilepsy in subject at risk after having received an epileptogenic insult), antiseizure (reduction of frequency and/or severity of seizures), and disease-modifying (alteration of the natural history of the disease) effects. An example of gene therapy aimed at producing antiepileptogenic effects is a combination therapy based on the supplementation of the neurotrophic factors brain-derived neurotrophic factor (BDNF) and fibroblast growth factor 2 (FGF-2). Antiseizure effects have been obtained by increasing the strength of inhibitory signals (by supplementing specific GABAA receptor subunits or inhibitory neuropeptides like galanin or neuropeptide Y) or by reducing the strength of excitatory signals (by knocking down NMDA receptor subunits). This review summarizes the results obtained to date using gene therapy in epilepsy models and discusses the challenges and the opportunities that this approach can offer for the treatment of human epilepsies. Enthalten in Elsevier Komiyama, Katsuya ELSEVIER Effect of morphology and molecular orientation on environmental water biodegradability of poly[( 2021 New York, NY [u.a.] (DE-627)ELV006838707 volume:38 year:2014 pages:125-130 extent:6 https://doi.org/10.1016/j.yebeh.2013.09.013 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 51.70 Polymerwerkstoffe Kunststoffe Werkstoffkunde VZ 35.80 Makromolekulare Chemie VZ AR 38 2014 125-130 6 045F 610 |
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10.1016/j.yebeh.2013.09.013 doi GBVA2014005000004.pica (DE-627)ELV017332699 (ELSEVIER)S1525-5050(13)00479-4 DE-627 ger DE-627 rakwb eng 610 610 DE-600 540 660 VZ 51.70 bkl 35.80 bkl Simonato, Michele verfasserin aut Gene therapy for epilepsy 2014transfer abstract 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Gene therapy may represent an effective alternative to standard pharmacological approaches for certain forms of epilepsy. Currently, the best candidates for this therapeutic approach appear to be epilepsies characterized by a focal lesion. Gene therapy has been attempted to produce antiepileptogenic (prevention of development of epilepsy in subject at risk after having received an epileptogenic insult), antiseizure (reduction of frequency and/or severity of seizures), and disease-modifying (alteration of the natural history of the disease) effects. An example of gene therapy aimed at producing antiepileptogenic effects is a combination therapy based on the supplementation of the neurotrophic factors brain-derived neurotrophic factor (BDNF) and fibroblast growth factor 2 (FGF-2). Antiseizure effects have been obtained by increasing the strength of inhibitory signals (by supplementing specific GABAA receptor subunits or inhibitory neuropeptides like galanin or neuropeptide Y) or by reducing the strength of excitatory signals (by knocking down NMDA receptor subunits). This review summarizes the results obtained to date using gene therapy in epilepsy models and discusses the challenges and the opportunities that this approach can offer for the treatment of human epilepsies. Gene therapy may represent an effective alternative to standard pharmacological approaches for certain forms of epilepsy. Currently, the best candidates for this therapeutic approach appear to be epilepsies characterized by a focal lesion. Gene therapy has been attempted to produce antiepileptogenic (prevention of development of epilepsy in subject at risk after having received an epileptogenic insult), antiseizure (reduction of frequency and/or severity of seizures), and disease-modifying (alteration of the natural history of the disease) effects. An example of gene therapy aimed at producing antiepileptogenic effects is a combination therapy based on the supplementation of the neurotrophic factors brain-derived neurotrophic factor (BDNF) and fibroblast growth factor 2 (FGF-2). Antiseizure effects have been obtained by increasing the strength of inhibitory signals (by supplementing specific GABAA receptor subunits or inhibitory neuropeptides like galanin or neuropeptide Y) or by reducing the strength of excitatory signals (by knocking down NMDA receptor subunits). This review summarizes the results obtained to date using gene therapy in epilepsy models and discusses the challenges and the opportunities that this approach can offer for the treatment of human epilepsies. Enthalten in Elsevier Komiyama, Katsuya ELSEVIER Effect of morphology and molecular orientation on environmental water biodegradability of poly[( 2021 New York, NY [u.a.] (DE-627)ELV006838707 volume:38 year:2014 pages:125-130 extent:6 https://doi.org/10.1016/j.yebeh.2013.09.013 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 51.70 Polymerwerkstoffe Kunststoffe Werkstoffkunde VZ 35.80 Makromolekulare Chemie VZ AR 38 2014 125-130 6 045F 610 |
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author |
Simonato, Michele |
spellingShingle |
Simonato, Michele ddc 610 ddc 540 bkl 51.70 bkl 35.80 Gene therapy for epilepsy |
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610 610 DE-600 540 660 VZ 51.70 bkl 35.80 bkl Gene therapy for epilepsy |
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Effect of morphology and molecular orientation on environmental water biodegradability of poly[( |
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Effect of morphology and molecular orientation on environmental water biodegradability of poly[( |
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gene therapy for epilepsy |
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Gene therapy for epilepsy |
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Gene therapy may represent an effective alternative to standard pharmacological approaches for certain forms of epilepsy. Currently, the best candidates for this therapeutic approach appear to be epilepsies characterized by a focal lesion. Gene therapy has been attempted to produce antiepileptogenic (prevention of development of epilepsy in subject at risk after having received an epileptogenic insult), antiseizure (reduction of frequency and/or severity of seizures), and disease-modifying (alteration of the natural history of the disease) effects. An example of gene therapy aimed at producing antiepileptogenic effects is a combination therapy based on the supplementation of the neurotrophic factors brain-derived neurotrophic factor (BDNF) and fibroblast growth factor 2 (FGF-2). Antiseizure effects have been obtained by increasing the strength of inhibitory signals (by supplementing specific GABAA receptor subunits or inhibitory neuropeptides like galanin or neuropeptide Y) or by reducing the strength of excitatory signals (by knocking down NMDA receptor subunits). This review summarizes the results obtained to date using gene therapy in epilepsy models and discusses the challenges and the opportunities that this approach can offer for the treatment of human epilepsies. |
abstractGer |
Gene therapy may represent an effective alternative to standard pharmacological approaches for certain forms of epilepsy. Currently, the best candidates for this therapeutic approach appear to be epilepsies characterized by a focal lesion. Gene therapy has been attempted to produce antiepileptogenic (prevention of development of epilepsy in subject at risk after having received an epileptogenic insult), antiseizure (reduction of frequency and/or severity of seizures), and disease-modifying (alteration of the natural history of the disease) effects. An example of gene therapy aimed at producing antiepileptogenic effects is a combination therapy based on the supplementation of the neurotrophic factors brain-derived neurotrophic factor (BDNF) and fibroblast growth factor 2 (FGF-2). Antiseizure effects have been obtained by increasing the strength of inhibitory signals (by supplementing specific GABAA receptor subunits or inhibitory neuropeptides like galanin or neuropeptide Y) or by reducing the strength of excitatory signals (by knocking down NMDA receptor subunits). This review summarizes the results obtained to date using gene therapy in epilepsy models and discusses the challenges and the opportunities that this approach can offer for the treatment of human epilepsies. |
abstract_unstemmed |
Gene therapy may represent an effective alternative to standard pharmacological approaches for certain forms of epilepsy. Currently, the best candidates for this therapeutic approach appear to be epilepsies characterized by a focal lesion. Gene therapy has been attempted to produce antiepileptogenic (prevention of development of epilepsy in subject at risk after having received an epileptogenic insult), antiseizure (reduction of frequency and/or severity of seizures), and disease-modifying (alteration of the natural history of the disease) effects. An example of gene therapy aimed at producing antiepileptogenic effects is a combination therapy based on the supplementation of the neurotrophic factors brain-derived neurotrophic factor (BDNF) and fibroblast growth factor 2 (FGF-2). Antiseizure effects have been obtained by increasing the strength of inhibitory signals (by supplementing specific GABAA receptor subunits or inhibitory neuropeptides like galanin or neuropeptide Y) or by reducing the strength of excitatory signals (by knocking down NMDA receptor subunits). This review summarizes the results obtained to date using gene therapy in epilepsy models and discusses the challenges and the opportunities that this approach can offer for the treatment of human epilepsies. |
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Gene therapy for epilepsy |
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