Disturbance of Iron Metabolism as a Contributing Factor to SN Hyperechogenicity in Parkinson’s Disease: Implications for Idiopathic and Monogenetic Forms
Abstract A number of investigations have provided evidence for a central role of iron in the pathogenesis of Parkinson’s disease (PD). Recently it could be demonstrated that iron related changes of the substantia nigra may be one important factor contributing to the hyperechogenicity typicall visual...
Ausführliche Beschreibung
Autor*in: |
Berg, Daniela [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2007 |
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Schlagwörter: |
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Übergeordnetes Werk: |
Enthalten in: Neurochemical research - Dordrecht [u.a.] : Springer Science + Business Media B.V, 1976, 32(2007), 10 vom: 28. Apr., Seite 1646-1654 |
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Übergeordnetes Werk: |
volume:32 ; year:2007 ; number:10 ; day:28 ; month:04 ; pages:1646-1654 |
Links: |
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DOI / URN: |
10.1007/s11064-007-9346-5 |
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Katalog-ID: |
SPR01623801X |
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245 | 1 | 0 | |a Disturbance of Iron Metabolism as a Contributing Factor to SN Hyperechogenicity in Parkinson’s Disease: Implications for Idiopathic and Monogenetic Forms |
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520 | |a Abstract A number of investigations have provided evidence for a central role of iron in the pathogenesis of Parkinson’s disease (PD). Recently it could be demonstrated that iron related changes of the substantia nigra may be one important factor contributing to the hyperechogenicity typicall visualized by transcranial sonography in idiopathic PD. Moreover, also patients with monogenetically caused PD show this hyperechogenicity, although to a lesser extent. According to numerous findings and experiments it seems plausible that iron also contributes to the pathophysiological cascades in the monogenetic forms of PD. Therefore, it is not only essential to acknowledge the pivotal role of iron for PD, but also to enhance the effort in finding therapeutic strategies to prevent the impact of iron on neurodegenerative processes. Moreover, early detection of subjects at risk is essential for the application of therapeutic strategies at a stage at which neuroprotection is still possible. | ||
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650 | 4 | |a Parkinson’s disease |7 (dpeaa)DE-He213 | |
650 | 4 | |a Monogenetic Parkinson’s disease |7 (dpeaa)DE-He213 | |
650 | 4 | |a Transcranial ultrasound |7 (dpeaa)DE-He213 | |
650 | 4 | |a Substantia nigra hyperechogenicity |7 (dpeaa)DE-He213 | |
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10.1007/s11064-007-9346-5 doi (DE-627)SPR01623801X (SPR)s11064-007-9346-5-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Berg, Daniela verfasserin aut Disturbance of Iron Metabolism as a Contributing Factor to SN Hyperechogenicity in Parkinson’s Disease: Implications for Idiopathic and Monogenetic Forms 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract A number of investigations have provided evidence for a central role of iron in the pathogenesis of Parkinson’s disease (PD). Recently it could be demonstrated that iron related changes of the substantia nigra may be one important factor contributing to the hyperechogenicity typicall visualized by transcranial sonography in idiopathic PD. Moreover, also patients with monogenetically caused PD show this hyperechogenicity, although to a lesser extent. According to numerous findings and experiments it seems plausible that iron also contributes to the pathophysiological cascades in the monogenetic forms of PD. Therefore, it is not only essential to acknowledge the pivotal role of iron for PD, but also to enhance the effort in finding therapeutic strategies to prevent the impact of iron on neurodegenerative processes. Moreover, early detection of subjects at risk is essential for the application of therapeutic strategies at a stage at which neuroprotection is still possible. Iron (dpeaa)DE-He213 Parkinson’s disease (dpeaa)DE-He213 Monogenetic Parkinson’s disease (dpeaa)DE-He213 Transcranial ultrasound (dpeaa)DE-He213 Substantia nigra hyperechogenicity (dpeaa)DE-He213 Enthalten in Neurochemical research Dordrecht [u.a.] : Springer Science + Business Media B.V, 1976 32(2007), 10 vom: 28. Apr., Seite 1646-1654 (DE-627)320587770 (DE-600)2018503-0 1573-6903 nnns volume:32 year:2007 number:10 day:28 month:04 pages:1646-1654 https://dx.doi.org/10.1007/s11064-007-9346-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 32 2007 10 28 04 1646-1654 |
spelling |
10.1007/s11064-007-9346-5 doi (DE-627)SPR01623801X (SPR)s11064-007-9346-5-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Berg, Daniela verfasserin aut Disturbance of Iron Metabolism as a Contributing Factor to SN Hyperechogenicity in Parkinson’s Disease: Implications for Idiopathic and Monogenetic Forms 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract A number of investigations have provided evidence for a central role of iron in the pathogenesis of Parkinson’s disease (PD). Recently it could be demonstrated that iron related changes of the substantia nigra may be one important factor contributing to the hyperechogenicity typicall visualized by transcranial sonography in idiopathic PD. Moreover, also patients with monogenetically caused PD show this hyperechogenicity, although to a lesser extent. According to numerous findings and experiments it seems plausible that iron also contributes to the pathophysiological cascades in the monogenetic forms of PD. Therefore, it is not only essential to acknowledge the pivotal role of iron for PD, but also to enhance the effort in finding therapeutic strategies to prevent the impact of iron on neurodegenerative processes. Moreover, early detection of subjects at risk is essential for the application of therapeutic strategies at a stage at which neuroprotection is still possible. Iron (dpeaa)DE-He213 Parkinson’s disease (dpeaa)DE-He213 Monogenetic Parkinson’s disease (dpeaa)DE-He213 Transcranial ultrasound (dpeaa)DE-He213 Substantia nigra hyperechogenicity (dpeaa)DE-He213 Enthalten in Neurochemical research Dordrecht [u.a.] : Springer Science + Business Media B.V, 1976 32(2007), 10 vom: 28. Apr., Seite 1646-1654 (DE-627)320587770 (DE-600)2018503-0 1573-6903 nnns volume:32 year:2007 number:10 day:28 month:04 pages:1646-1654 https://dx.doi.org/10.1007/s11064-007-9346-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 32 2007 10 28 04 1646-1654 |
allfields_unstemmed |
10.1007/s11064-007-9346-5 doi (DE-627)SPR01623801X (SPR)s11064-007-9346-5-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Berg, Daniela verfasserin aut Disturbance of Iron Metabolism as a Contributing Factor to SN Hyperechogenicity in Parkinson’s Disease: Implications for Idiopathic and Monogenetic Forms 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract A number of investigations have provided evidence for a central role of iron in the pathogenesis of Parkinson’s disease (PD). Recently it could be demonstrated that iron related changes of the substantia nigra may be one important factor contributing to the hyperechogenicity typicall visualized by transcranial sonography in idiopathic PD. Moreover, also patients with monogenetically caused PD show this hyperechogenicity, although to a lesser extent. According to numerous findings and experiments it seems plausible that iron also contributes to the pathophysiological cascades in the monogenetic forms of PD. Therefore, it is not only essential to acknowledge the pivotal role of iron for PD, but also to enhance the effort in finding therapeutic strategies to prevent the impact of iron on neurodegenerative processes. Moreover, early detection of subjects at risk is essential for the application of therapeutic strategies at a stage at which neuroprotection is still possible. Iron (dpeaa)DE-He213 Parkinson’s disease (dpeaa)DE-He213 Monogenetic Parkinson’s disease (dpeaa)DE-He213 Transcranial ultrasound (dpeaa)DE-He213 Substantia nigra hyperechogenicity (dpeaa)DE-He213 Enthalten in Neurochemical research Dordrecht [u.a.] : Springer Science + Business Media B.V, 1976 32(2007), 10 vom: 28. Apr., Seite 1646-1654 (DE-627)320587770 (DE-600)2018503-0 1573-6903 nnns volume:32 year:2007 number:10 day:28 month:04 pages:1646-1654 https://dx.doi.org/10.1007/s11064-007-9346-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 32 2007 10 28 04 1646-1654 |
allfieldsGer |
10.1007/s11064-007-9346-5 doi (DE-627)SPR01623801X (SPR)s11064-007-9346-5-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Berg, Daniela verfasserin aut Disturbance of Iron Metabolism as a Contributing Factor to SN Hyperechogenicity in Parkinson’s Disease: Implications for Idiopathic and Monogenetic Forms 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract A number of investigations have provided evidence for a central role of iron in the pathogenesis of Parkinson’s disease (PD). Recently it could be demonstrated that iron related changes of the substantia nigra may be one important factor contributing to the hyperechogenicity typicall visualized by transcranial sonography in idiopathic PD. Moreover, also patients with monogenetically caused PD show this hyperechogenicity, although to a lesser extent. According to numerous findings and experiments it seems plausible that iron also contributes to the pathophysiological cascades in the monogenetic forms of PD. Therefore, it is not only essential to acknowledge the pivotal role of iron for PD, but also to enhance the effort in finding therapeutic strategies to prevent the impact of iron on neurodegenerative processes. Moreover, early detection of subjects at risk is essential for the application of therapeutic strategies at a stage at which neuroprotection is still possible. Iron (dpeaa)DE-He213 Parkinson’s disease (dpeaa)DE-He213 Monogenetic Parkinson’s disease (dpeaa)DE-He213 Transcranial ultrasound (dpeaa)DE-He213 Substantia nigra hyperechogenicity (dpeaa)DE-He213 Enthalten in Neurochemical research Dordrecht [u.a.] : Springer Science + Business Media B.V, 1976 32(2007), 10 vom: 28. Apr., Seite 1646-1654 (DE-627)320587770 (DE-600)2018503-0 1573-6903 nnns volume:32 year:2007 number:10 day:28 month:04 pages:1646-1654 https://dx.doi.org/10.1007/s11064-007-9346-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 32 2007 10 28 04 1646-1654 |
allfieldsSound |
10.1007/s11064-007-9346-5 doi (DE-627)SPR01623801X (SPR)s11064-007-9346-5-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Berg, Daniela verfasserin aut Disturbance of Iron Metabolism as a Contributing Factor to SN Hyperechogenicity in Parkinson’s Disease: Implications for Idiopathic and Monogenetic Forms 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract A number of investigations have provided evidence for a central role of iron in the pathogenesis of Parkinson’s disease (PD). Recently it could be demonstrated that iron related changes of the substantia nigra may be one important factor contributing to the hyperechogenicity typicall visualized by transcranial sonography in idiopathic PD. Moreover, also patients with monogenetically caused PD show this hyperechogenicity, although to a lesser extent. According to numerous findings and experiments it seems plausible that iron also contributes to the pathophysiological cascades in the monogenetic forms of PD. Therefore, it is not only essential to acknowledge the pivotal role of iron for PD, but also to enhance the effort in finding therapeutic strategies to prevent the impact of iron on neurodegenerative processes. Moreover, early detection of subjects at risk is essential for the application of therapeutic strategies at a stage at which neuroprotection is still possible. Iron (dpeaa)DE-He213 Parkinson’s disease (dpeaa)DE-He213 Monogenetic Parkinson’s disease (dpeaa)DE-He213 Transcranial ultrasound (dpeaa)DE-He213 Substantia nigra hyperechogenicity (dpeaa)DE-He213 Enthalten in Neurochemical research Dordrecht [u.a.] : Springer Science + Business Media B.V, 1976 32(2007), 10 vom: 28. Apr., Seite 1646-1654 (DE-627)320587770 (DE-600)2018503-0 1573-6903 nnns volume:32 year:2007 number:10 day:28 month:04 pages:1646-1654 https://dx.doi.org/10.1007/s11064-007-9346-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 32 2007 10 28 04 1646-1654 |
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Enthalten in Neurochemical research 32(2007), 10 vom: 28. Apr., Seite 1646-1654 volume:32 year:2007 number:10 day:28 month:04 pages:1646-1654 |
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Iron Parkinson’s disease Monogenetic Parkinson’s disease Transcranial ultrasound Substantia nigra hyperechogenicity |
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Berg, Daniela @@aut@@ |
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Berg, Daniela |
spellingShingle |
Berg, Daniela ddc 610 bkl 44.90 misc Iron misc Parkinson’s disease misc Monogenetic Parkinson’s disease misc Transcranial ultrasound misc Substantia nigra hyperechogenicity Disturbance of Iron Metabolism as a Contributing Factor to SN Hyperechogenicity in Parkinson’s Disease: Implications for Idiopathic and Monogenetic Forms |
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610 ASE 44.90 bkl Disturbance of Iron Metabolism as a Contributing Factor to SN Hyperechogenicity in Parkinson’s Disease: Implications for Idiopathic and Monogenetic Forms Iron (dpeaa)DE-He213 Parkinson’s disease (dpeaa)DE-He213 Monogenetic Parkinson’s disease (dpeaa)DE-He213 Transcranial ultrasound (dpeaa)DE-He213 Substantia nigra hyperechogenicity (dpeaa)DE-He213 |
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ddc 610 bkl 44.90 misc Iron misc Parkinson’s disease misc Monogenetic Parkinson’s disease misc Transcranial ultrasound misc Substantia nigra hyperechogenicity |
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ddc 610 bkl 44.90 misc Iron misc Parkinson’s disease misc Monogenetic Parkinson’s disease misc Transcranial ultrasound misc Substantia nigra hyperechogenicity |
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title |
Disturbance of Iron Metabolism as a Contributing Factor to SN Hyperechogenicity in Parkinson’s Disease: Implications for Idiopathic and Monogenetic Forms |
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Disturbance of Iron Metabolism as a Contributing Factor to SN Hyperechogenicity in Parkinson’s Disease: Implications for Idiopathic and Monogenetic Forms |
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disturbance of iron metabolism as a contributing factor to sn hyperechogenicity in parkinson’s disease: implications for idiopathic and monogenetic forms |
title_auth |
Disturbance of Iron Metabolism as a Contributing Factor to SN Hyperechogenicity in Parkinson’s Disease: Implications for Idiopathic and Monogenetic Forms |
abstract |
Abstract A number of investigations have provided evidence for a central role of iron in the pathogenesis of Parkinson’s disease (PD). Recently it could be demonstrated that iron related changes of the substantia nigra may be one important factor contributing to the hyperechogenicity typicall visualized by transcranial sonography in idiopathic PD. Moreover, also patients with monogenetically caused PD show this hyperechogenicity, although to a lesser extent. According to numerous findings and experiments it seems plausible that iron also contributes to the pathophysiological cascades in the monogenetic forms of PD. Therefore, it is not only essential to acknowledge the pivotal role of iron for PD, but also to enhance the effort in finding therapeutic strategies to prevent the impact of iron on neurodegenerative processes. Moreover, early detection of subjects at risk is essential for the application of therapeutic strategies at a stage at which neuroprotection is still possible. |
abstractGer |
Abstract A number of investigations have provided evidence for a central role of iron in the pathogenesis of Parkinson’s disease (PD). Recently it could be demonstrated that iron related changes of the substantia nigra may be one important factor contributing to the hyperechogenicity typicall visualized by transcranial sonography in idiopathic PD. Moreover, also patients with monogenetically caused PD show this hyperechogenicity, although to a lesser extent. According to numerous findings and experiments it seems plausible that iron also contributes to the pathophysiological cascades in the monogenetic forms of PD. Therefore, it is not only essential to acknowledge the pivotal role of iron for PD, but also to enhance the effort in finding therapeutic strategies to prevent the impact of iron on neurodegenerative processes. Moreover, early detection of subjects at risk is essential for the application of therapeutic strategies at a stage at which neuroprotection is still possible. |
abstract_unstemmed |
Abstract A number of investigations have provided evidence for a central role of iron in the pathogenesis of Parkinson’s disease (PD). Recently it could be demonstrated that iron related changes of the substantia nigra may be one important factor contributing to the hyperechogenicity typicall visualized by transcranial sonography in idiopathic PD. Moreover, also patients with monogenetically caused PD show this hyperechogenicity, although to a lesser extent. According to numerous findings and experiments it seems plausible that iron also contributes to the pathophysiological cascades in the monogenetic forms of PD. Therefore, it is not only essential to acknowledge the pivotal role of iron for PD, but also to enhance the effort in finding therapeutic strategies to prevent the impact of iron on neurodegenerative processes. Moreover, early detection of subjects at risk is essential for the application of therapeutic strategies at a stage at which neuroprotection is still possible. |
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container_issue |
10 |
title_short |
Disturbance of Iron Metabolism as a Contributing Factor to SN Hyperechogenicity in Parkinson’s Disease: Implications for Idiopathic and Monogenetic Forms |
url |
https://dx.doi.org/10.1007/s11064-007-9346-5 |
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doi_str |
10.1007/s11064-007-9346-5 |
up_date |
2024-07-03T21:46:32.363Z |
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