Multiple system atrophy as emerging template for accelerated drug discovery in α-synucleinopathies
There is evidence that the α-synucleinopathies Parkinson's disease (PD) and the Parkinson variant of multiple system atrophy (MSA-P) overlap at multiple levels. Both disorders are characterized by deposition of abnormally phosphorylated fibrillar α-synuclein within the central nervous system su...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Krismer, Florian [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2014transfer abstract |
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| Umfang: |
7 |
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| Übergeordnetes Werk: |
Enthalten in: Parkinsonism & related disorders - Aral, Efecan ELSEVIER, 2022, official journal of the World Federation of Neurology Research Committee on Parkinsonism and Related Disorders, Amsterdam [u.a.] |
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| Übergeordnetes Werk: |
volume:20 ; year:2014 ; number:8 ; pages:793-799 ; extent:7 |
| Links: |
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| DOI / URN: |
10.1016/j.parkreldis.2014.05.005 |
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| 520 | |a There is evidence that the α-synucleinopathies Parkinson's disease (PD) and the Parkinson variant of multiple system atrophy (MSA-P) overlap at multiple levels. Both disorders are characterized by deposition of abnormally phosphorylated fibrillar α-synuclein within the central nervous system suggesting shared pathophysiological mechanisms. Despite the considerable clinical overlap in the early disease stages, MSA-P, in contrast to PD, is fatal and rapidly progressive. Moreover recent clinical studies have shown that surrogate markers of disease progression can be quantified easily and may reliably depict the rapid course of MSA. We therefore posit that, MSA-P may be exploited as a filter barrier in the development of disease-modifying therapeutic strategies targeting common pathophysiological mechanisms of α-synucleinopathies. This approach might reduce the number of negative phase III clinical trials, and, in turn, shift the available resources to earlier development stages, thereby increasing the number of candidate compounds validated. | ||
| 520 | |a There is evidence that the α-synucleinopathies Parkinson's disease (PD) and the Parkinson variant of multiple system atrophy (MSA-P) overlap at multiple levels. Both disorders are characterized by deposition of abnormally phosphorylated fibrillar α-synuclein within the central nervous system suggesting shared pathophysiological mechanisms. Despite the considerable clinical overlap in the early disease stages, MSA-P, in contrast to PD, is fatal and rapidly progressive. Moreover recent clinical studies have shown that surrogate markers of disease progression can be quantified easily and may reliably depict the rapid course of MSA. We therefore posit that, MSA-P may be exploited as a filter barrier in the development of disease-modifying therapeutic strategies targeting common pathophysiological mechanisms of α-synucleinopathies. This approach might reduce the number of negative phase III clinical trials, and, in turn, shift the available resources to earlier development stages, thereby increasing the number of candidate compounds validated. | ||
| 650 | 7 | |a Parkinson's disease |2 Elsevier | |
| 650 | 7 | |a Multiple system atrophy |2 Elsevier | |
| 650 | 7 | |a Synucleinopathies |2 Elsevier | |
| 650 | 7 | |a Drug development |2 Elsevier | |
| 700 | 1 | |a Jellinger, Kurt A. |4 oth | |
| 700 | 1 | |a Scholz, Sonja W. |4 oth | |
| 700 | 1 | |a Seppi, Klaus |4 oth | |
| 700 | 1 | |a Stefanova, Nadia |4 oth | |
| 700 | 1 | |a Antonini, Angelo |4 oth | |
| 700 | 1 | |a Poewe, Werner |4 oth | |
| 700 | 1 | |a Wenning, Gregor K. |4 oth | |
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10.1016/j.parkreldis.2014.05.005 doi GBVA2014019000004.pica (DE-627)ELV028378385 (ELSEVIER)S1353-8020(14)00194-1 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 42.13 bkl 44.33 bkl Krismer, Florian verfasserin aut Multiple system atrophy as emerging template for accelerated drug discovery in α-synucleinopathies 2014transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier There is evidence that the α-synucleinopathies Parkinson's disease (PD) and the Parkinson variant of multiple system atrophy (MSA-P) overlap at multiple levels. Both disorders are characterized by deposition of abnormally phosphorylated fibrillar α-synuclein within the central nervous system suggesting shared pathophysiological mechanisms. Despite the considerable clinical overlap in the early disease stages, MSA-P, in contrast to PD, is fatal and rapidly progressive. Moreover recent clinical studies have shown that surrogate markers of disease progression can be quantified easily and may reliably depict the rapid course of MSA. We therefore posit that, MSA-P may be exploited as a filter barrier in the development of disease-modifying therapeutic strategies targeting common pathophysiological mechanisms of α-synucleinopathies. This approach might reduce the number of negative phase III clinical trials, and, in turn, shift the available resources to earlier development stages, thereby increasing the number of candidate compounds validated. There is evidence that the α-synucleinopathies Parkinson's disease (PD) and the Parkinson variant of multiple system atrophy (MSA-P) overlap at multiple levels. Both disorders are characterized by deposition of abnormally phosphorylated fibrillar α-synuclein within the central nervous system suggesting shared pathophysiological mechanisms. Despite the considerable clinical overlap in the early disease stages, MSA-P, in contrast to PD, is fatal and rapidly progressive. Moreover recent clinical studies have shown that surrogate markers of disease progression can be quantified easily and may reliably depict the rapid course of MSA. We therefore posit that, MSA-P may be exploited as a filter barrier in the development of disease-modifying therapeutic strategies targeting common pathophysiological mechanisms of α-synucleinopathies. This approach might reduce the number of negative phase III clinical trials, and, in turn, shift the available resources to earlier development stages, thereby increasing the number of candidate compounds validated. Parkinson's disease Elsevier Multiple system atrophy Elsevier Synucleinopathies Elsevier Drug development Elsevier Jellinger, Kurt A. oth Scholz, Sonja W. oth Seppi, Klaus oth Stefanova, Nadia oth Antonini, Angelo oth Poewe, Werner oth Wenning, Gregor K. oth Enthalten in Elsevier Science Aral, Efecan ELSEVIER Parkinsonism & related disorders 2022 official journal of the World Federation of Neurology Research Committee on Parkinsonism and Related Disorders Amsterdam [u.a.] (DE-627)ELV009218491 volume:20 year:2014 number:8 pages:793-799 extent:7 https://doi.org/10.1016/j.parkreldis.2014.05.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 42.13 Molekularbiologie VZ 44.33 Physiologische Chemie VZ AR 20 2014 8 793-799 7 045F 610 |
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10.1016/j.parkreldis.2014.05.005 doi GBVA2014019000004.pica (DE-627)ELV028378385 (ELSEVIER)S1353-8020(14)00194-1 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 42.13 bkl 44.33 bkl Krismer, Florian verfasserin aut Multiple system atrophy as emerging template for accelerated drug discovery in α-synucleinopathies 2014transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier There is evidence that the α-synucleinopathies Parkinson's disease (PD) and the Parkinson variant of multiple system atrophy (MSA-P) overlap at multiple levels. Both disorders are characterized by deposition of abnormally phosphorylated fibrillar α-synuclein within the central nervous system suggesting shared pathophysiological mechanisms. Despite the considerable clinical overlap in the early disease stages, MSA-P, in contrast to PD, is fatal and rapidly progressive. Moreover recent clinical studies have shown that surrogate markers of disease progression can be quantified easily and may reliably depict the rapid course of MSA. We therefore posit that, MSA-P may be exploited as a filter barrier in the development of disease-modifying therapeutic strategies targeting common pathophysiological mechanisms of α-synucleinopathies. This approach might reduce the number of negative phase III clinical trials, and, in turn, shift the available resources to earlier development stages, thereby increasing the number of candidate compounds validated. There is evidence that the α-synucleinopathies Parkinson's disease (PD) and the Parkinson variant of multiple system atrophy (MSA-P) overlap at multiple levels. Both disorders are characterized by deposition of abnormally phosphorylated fibrillar α-synuclein within the central nervous system suggesting shared pathophysiological mechanisms. Despite the considerable clinical overlap in the early disease stages, MSA-P, in contrast to PD, is fatal and rapidly progressive. Moreover recent clinical studies have shown that surrogate markers of disease progression can be quantified easily and may reliably depict the rapid course of MSA. We therefore posit that, MSA-P may be exploited as a filter barrier in the development of disease-modifying therapeutic strategies targeting common pathophysiological mechanisms of α-synucleinopathies. This approach might reduce the number of negative phase III clinical trials, and, in turn, shift the available resources to earlier development stages, thereby increasing the number of candidate compounds validated. Parkinson's disease Elsevier Multiple system atrophy Elsevier Synucleinopathies Elsevier Drug development Elsevier Jellinger, Kurt A. oth Scholz, Sonja W. oth Seppi, Klaus oth Stefanova, Nadia oth Antonini, Angelo oth Poewe, Werner oth Wenning, Gregor K. oth Enthalten in Elsevier Science Aral, Efecan ELSEVIER Parkinsonism & related disorders 2022 official journal of the World Federation of Neurology Research Committee on Parkinsonism and Related Disorders Amsterdam [u.a.] (DE-627)ELV009218491 volume:20 year:2014 number:8 pages:793-799 extent:7 https://doi.org/10.1016/j.parkreldis.2014.05.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 42.13 Molekularbiologie VZ 44.33 Physiologische Chemie VZ AR 20 2014 8 793-799 7 045F 610 |
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10.1016/j.parkreldis.2014.05.005 doi GBVA2014019000004.pica (DE-627)ELV028378385 (ELSEVIER)S1353-8020(14)00194-1 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 42.13 bkl 44.33 bkl Krismer, Florian verfasserin aut Multiple system atrophy as emerging template for accelerated drug discovery in α-synucleinopathies 2014transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier There is evidence that the α-synucleinopathies Parkinson's disease (PD) and the Parkinson variant of multiple system atrophy (MSA-P) overlap at multiple levels. Both disorders are characterized by deposition of abnormally phosphorylated fibrillar α-synuclein within the central nervous system suggesting shared pathophysiological mechanisms. Despite the considerable clinical overlap in the early disease stages, MSA-P, in contrast to PD, is fatal and rapidly progressive. Moreover recent clinical studies have shown that surrogate markers of disease progression can be quantified easily and may reliably depict the rapid course of MSA. We therefore posit that, MSA-P may be exploited as a filter barrier in the development of disease-modifying therapeutic strategies targeting common pathophysiological mechanisms of α-synucleinopathies. This approach might reduce the number of negative phase III clinical trials, and, in turn, shift the available resources to earlier development stages, thereby increasing the number of candidate compounds validated. There is evidence that the α-synucleinopathies Parkinson's disease (PD) and the Parkinson variant of multiple system atrophy (MSA-P) overlap at multiple levels. Both disorders are characterized by deposition of abnormally phosphorylated fibrillar α-synuclein within the central nervous system suggesting shared pathophysiological mechanisms. Despite the considerable clinical overlap in the early disease stages, MSA-P, in contrast to PD, is fatal and rapidly progressive. Moreover recent clinical studies have shown that surrogate markers of disease progression can be quantified easily and may reliably depict the rapid course of MSA. We therefore posit that, MSA-P may be exploited as a filter barrier in the development of disease-modifying therapeutic strategies targeting common pathophysiological mechanisms of α-synucleinopathies. This approach might reduce the number of negative phase III clinical trials, and, in turn, shift the available resources to earlier development stages, thereby increasing the number of candidate compounds validated. Parkinson's disease Elsevier Multiple system atrophy Elsevier Synucleinopathies Elsevier Drug development Elsevier Jellinger, Kurt A. oth Scholz, Sonja W. oth Seppi, Klaus oth Stefanova, Nadia oth Antonini, Angelo oth Poewe, Werner oth Wenning, Gregor K. oth Enthalten in Elsevier Science Aral, Efecan ELSEVIER Parkinsonism & related disorders 2022 official journal of the World Federation of Neurology Research Committee on Parkinsonism and Related Disorders Amsterdam [u.a.] (DE-627)ELV009218491 volume:20 year:2014 number:8 pages:793-799 extent:7 https://doi.org/10.1016/j.parkreldis.2014.05.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 42.13 Molekularbiologie VZ 44.33 Physiologische Chemie VZ AR 20 2014 8 793-799 7 045F 610 |
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10.1016/j.parkreldis.2014.05.005 doi GBVA2014019000004.pica (DE-627)ELV028378385 (ELSEVIER)S1353-8020(14)00194-1 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 42.13 bkl 44.33 bkl Krismer, Florian verfasserin aut Multiple system atrophy as emerging template for accelerated drug discovery in α-synucleinopathies 2014transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier There is evidence that the α-synucleinopathies Parkinson's disease (PD) and the Parkinson variant of multiple system atrophy (MSA-P) overlap at multiple levels. Both disorders are characterized by deposition of abnormally phosphorylated fibrillar α-synuclein within the central nervous system suggesting shared pathophysiological mechanisms. Despite the considerable clinical overlap in the early disease stages, MSA-P, in contrast to PD, is fatal and rapidly progressive. Moreover recent clinical studies have shown that surrogate markers of disease progression can be quantified easily and may reliably depict the rapid course of MSA. We therefore posit that, MSA-P may be exploited as a filter barrier in the development of disease-modifying therapeutic strategies targeting common pathophysiological mechanisms of α-synucleinopathies. This approach might reduce the number of negative phase III clinical trials, and, in turn, shift the available resources to earlier development stages, thereby increasing the number of candidate compounds validated. There is evidence that the α-synucleinopathies Parkinson's disease (PD) and the Parkinson variant of multiple system atrophy (MSA-P) overlap at multiple levels. Both disorders are characterized by deposition of abnormally phosphorylated fibrillar α-synuclein within the central nervous system suggesting shared pathophysiological mechanisms. Despite the considerable clinical overlap in the early disease stages, MSA-P, in contrast to PD, is fatal and rapidly progressive. Moreover recent clinical studies have shown that surrogate markers of disease progression can be quantified easily and may reliably depict the rapid course of MSA. We therefore posit that, MSA-P may be exploited as a filter barrier in the development of disease-modifying therapeutic strategies targeting common pathophysiological mechanisms of α-synucleinopathies. This approach might reduce the number of negative phase III clinical trials, and, in turn, shift the available resources to earlier development stages, thereby increasing the number of candidate compounds validated. Parkinson's disease Elsevier Multiple system atrophy Elsevier Synucleinopathies Elsevier Drug development Elsevier Jellinger, Kurt A. oth Scholz, Sonja W. oth Seppi, Klaus oth Stefanova, Nadia oth Antonini, Angelo oth Poewe, Werner oth Wenning, Gregor K. oth Enthalten in Elsevier Science Aral, Efecan ELSEVIER Parkinsonism & related disorders 2022 official journal of the World Federation of Neurology Research Committee on Parkinsonism and Related Disorders Amsterdam [u.a.] (DE-627)ELV009218491 volume:20 year:2014 number:8 pages:793-799 extent:7 https://doi.org/10.1016/j.parkreldis.2014.05.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 42.13 Molekularbiologie VZ 44.33 Physiologische Chemie VZ AR 20 2014 8 793-799 7 045F 610 |
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10.1016/j.parkreldis.2014.05.005 doi GBVA2014019000004.pica (DE-627)ELV028378385 (ELSEVIER)S1353-8020(14)00194-1 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 42.13 bkl 44.33 bkl Krismer, Florian verfasserin aut Multiple system atrophy as emerging template for accelerated drug discovery in α-synucleinopathies 2014transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier There is evidence that the α-synucleinopathies Parkinson's disease (PD) and the Parkinson variant of multiple system atrophy (MSA-P) overlap at multiple levels. Both disorders are characterized by deposition of abnormally phosphorylated fibrillar α-synuclein within the central nervous system suggesting shared pathophysiological mechanisms. Despite the considerable clinical overlap in the early disease stages, MSA-P, in contrast to PD, is fatal and rapidly progressive. Moreover recent clinical studies have shown that surrogate markers of disease progression can be quantified easily and may reliably depict the rapid course of MSA. We therefore posit that, MSA-P may be exploited as a filter barrier in the development of disease-modifying therapeutic strategies targeting common pathophysiological mechanisms of α-synucleinopathies. This approach might reduce the number of negative phase III clinical trials, and, in turn, shift the available resources to earlier development stages, thereby increasing the number of candidate compounds validated. There is evidence that the α-synucleinopathies Parkinson's disease (PD) and the Parkinson variant of multiple system atrophy (MSA-P) overlap at multiple levels. Both disorders are characterized by deposition of abnormally phosphorylated fibrillar α-synuclein within the central nervous system suggesting shared pathophysiological mechanisms. Despite the considerable clinical overlap in the early disease stages, MSA-P, in contrast to PD, is fatal and rapidly progressive. Moreover recent clinical studies have shown that surrogate markers of disease progression can be quantified easily and may reliably depict the rapid course of MSA. We therefore posit that, MSA-P may be exploited as a filter barrier in the development of disease-modifying therapeutic strategies targeting common pathophysiological mechanisms of α-synucleinopathies. This approach might reduce the number of negative phase III clinical trials, and, in turn, shift the available resources to earlier development stages, thereby increasing the number of candidate compounds validated. Parkinson's disease Elsevier Multiple system atrophy Elsevier Synucleinopathies Elsevier Drug development Elsevier Jellinger, Kurt A. oth Scholz, Sonja W. oth Seppi, Klaus oth Stefanova, Nadia oth Antonini, Angelo oth Poewe, Werner oth Wenning, Gregor K. oth Enthalten in Elsevier Science Aral, Efecan ELSEVIER Parkinsonism & related disorders 2022 official journal of the World Federation of Neurology Research Committee on Parkinsonism and Related Disorders Amsterdam [u.a.] (DE-627)ELV009218491 volume:20 year:2014 number:8 pages:793-799 extent:7 https://doi.org/10.1016/j.parkreldis.2014.05.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 42.13 Molekularbiologie VZ 44.33 Physiologische Chemie VZ AR 20 2014 8 793-799 7 045F 610 |
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Enthalten in Parkinsonism & related disorders Amsterdam [u.a.] volume:20 year:2014 number:8 pages:793-799 extent:7 |
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Multiple system atrophy as emerging template for accelerated drug discovery in α-synucleinopathies |
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There is evidence that the α-synucleinopathies Parkinson's disease (PD) and the Parkinson variant of multiple system atrophy (MSA-P) overlap at multiple levels. Both disorders are characterized by deposition of abnormally phosphorylated fibrillar α-synuclein within the central nervous system suggesting shared pathophysiological mechanisms. Despite the considerable clinical overlap in the early disease stages, MSA-P, in contrast to PD, is fatal and rapidly progressive. Moreover recent clinical studies have shown that surrogate markers of disease progression can be quantified easily and may reliably depict the rapid course of MSA. We therefore posit that, MSA-P may be exploited as a filter barrier in the development of disease-modifying therapeutic strategies targeting common pathophysiological mechanisms of α-synucleinopathies. This approach might reduce the number of negative phase III clinical trials, and, in turn, shift the available resources to earlier development stages, thereby increasing the number of candidate compounds validated. |
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There is evidence that the α-synucleinopathies Parkinson's disease (PD) and the Parkinson variant of multiple system atrophy (MSA-P) overlap at multiple levels. Both disorders are characterized by deposition of abnormally phosphorylated fibrillar α-synuclein within the central nervous system suggesting shared pathophysiological mechanisms. Despite the considerable clinical overlap in the early disease stages, MSA-P, in contrast to PD, is fatal and rapidly progressive. Moreover recent clinical studies have shown that surrogate markers of disease progression can be quantified easily and may reliably depict the rapid course of MSA. We therefore posit that, MSA-P may be exploited as a filter barrier in the development of disease-modifying therapeutic strategies targeting common pathophysiological mechanisms of α-synucleinopathies. This approach might reduce the number of negative phase III clinical trials, and, in turn, shift the available resources to earlier development stages, thereby increasing the number of candidate compounds validated. |
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There is evidence that the α-synucleinopathies Parkinson's disease (PD) and the Parkinson variant of multiple system atrophy (MSA-P) overlap at multiple levels. Both disorders are characterized by deposition of abnormally phosphorylated fibrillar α-synuclein within the central nervous system suggesting shared pathophysiological mechanisms. Despite the considerable clinical overlap in the early disease stages, MSA-P, in contrast to PD, is fatal and rapidly progressive. Moreover recent clinical studies have shown that surrogate markers of disease progression can be quantified easily and may reliably depict the rapid course of MSA. We therefore posit that, MSA-P may be exploited as a filter barrier in the development of disease-modifying therapeutic strategies targeting common pathophysiological mechanisms of α-synucleinopathies. This approach might reduce the number of negative phase III clinical trials, and, in turn, shift the available resources to earlier development stages, thereby increasing the number of candidate compounds validated. |
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