Intensive protein synthesis in neurons and phosphorylation of beta-amyloid precursor protein and tau-protein are triggering factors of neuronal amyloidosis and Alzheimer’s disease
Abstract Studies of Alzheimer’s disease have become particularly important and attract now much attention of scientists all over the world due to worldwide dissemination of this dangerous disorder. Causes of this pathology still remain unknown, while the final image, originally obtained on microscop...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Maltsev, A. V. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2013 |
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| Schlagwörter: |
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| Anmerkung: |
© Pleiades Publishing, Ltd. 2013 |
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| Übergeordnetes Werk: |
Enthalten in: Biochemistry (Moscow) - Dordrecht [u.a.] : Springer Science + Business Media B.V, 2007, 7(2013), 4 vom: Okt., Seite 278-293 |
|---|---|
| Übergeordnetes Werk: |
volume:7 ; year:2013 ; number:4 ; month:10 ; pages:278-293 |
| Links: |
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| DOI / URN: |
10.1134/S1990750813040057 |
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| Katalog-ID: |
SPR022600396 |
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| 100 | 1 | |a Maltsev, A. V. |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Intensive protein synthesis in neurons and phosphorylation of beta-amyloid precursor protein and tau-protein are triggering factors of neuronal amyloidosis and Alzheimer’s disease |
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| 520 | |a Abstract Studies of Alzheimer’s disease have become particularly important and attract now much attention of scientists all over the world due to worldwide dissemination of this dangerous disorder. Causes of this pathology still remain unknown, while the final image, originally obtained on microscopic brain sections from patients with this disease more than a hundred years ago, is well familiar to clinicians. This includes deposition of amyloid-β (Aβ) in the brain tissue of senile plaques and fibrils. Many authors believe that the deposition of Aβ provokes secondary neuronal changes, responsible for death of neurons. Other authors associate the death of neurons with hyperphosphorylation of tau-proteins, which form neurofibrillar tangles inside nerve cells and cause their death. Creation of methods of preclinical diagnostics and effective treatment of Alzheimer’s disease requires novel knowledge: on the nature of triggering factors of sporadic forms of Alzheimer’s disease, on cause-effect relationships of phosphorylation of amyloid precursor protein with formation of pathogenic beta-amyloids, on the relationship between these factors underlying tau-protein hyperphosphorylation and neuron death. In this review we have analyzed reports describing increased intensity of protein synthesis in neurons under normal and various stress conditions, possibility of development of energy imbalance of neurons and activation of their protective systems. Phosphorylation and hyperphosphorylation of tau-proteins is also tightly associated with protective mechanisms of cells and with processes of evacuation of phosphates, adenosine monophosphates and pyrophosphates from the region of protein synthesis. Prolonged highly intensive protein synthesis causes overload of protective mechanisms and impairments in concerted metabolic processes. This leads to neuronal dysfunction, transport collapse, and death of neurons. | ||
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| 650 | 4 | |a amyloid precursor protein |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a neuronal death |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a protein synthesis |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a tau-protein |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a phosphorylation |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Dovidchenko, N. V. |4 aut | |
| 700 | 1 | |a Uteshev, V. K. |4 aut | |
| 700 | 1 | |a Sokolik, V. V. |4 aut | |
| 700 | 1 | |a Shtang, O. M. |4 aut | |
| 700 | 1 | |a Yakushin, M. A. |4 aut | |
| 700 | 1 | |a Sokolova, N. M. |4 aut | |
| 700 | 1 | |a Surin, A. K. |4 aut | |
| 700 | 1 | |a Galzitskaya, O. V. |4 aut | |
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10.1134/S1990750813040057 doi (DE-627)SPR022600396 (SPR)S1990750813040057-e DE-627 ger DE-627 rakwb eng Maltsev, A. V. verfasserin aut Intensive protein synthesis in neurons and phosphorylation of beta-amyloid precursor protein and tau-protein are triggering factors of neuronal amyloidosis and Alzheimer’s disease 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Pleiades Publishing, Ltd. 2013 Abstract Studies of Alzheimer’s disease have become particularly important and attract now much attention of scientists all over the world due to worldwide dissemination of this dangerous disorder. Causes of this pathology still remain unknown, while the final image, originally obtained on microscopic brain sections from patients with this disease more than a hundred years ago, is well familiar to clinicians. This includes deposition of amyloid-β (Aβ) in the brain tissue of senile plaques and fibrils. Many authors believe that the deposition of Aβ provokes secondary neuronal changes, responsible for death of neurons. Other authors associate the death of neurons with hyperphosphorylation of tau-proteins, which form neurofibrillar tangles inside nerve cells and cause their death. Creation of methods of preclinical diagnostics and effective treatment of Alzheimer’s disease requires novel knowledge: on the nature of triggering factors of sporadic forms of Alzheimer’s disease, on cause-effect relationships of phosphorylation of amyloid precursor protein with formation of pathogenic beta-amyloids, on the relationship between these factors underlying tau-protein hyperphosphorylation and neuron death. In this review we have analyzed reports describing increased intensity of protein synthesis in neurons under normal and various stress conditions, possibility of development of energy imbalance of neurons and activation of their protective systems. Phosphorylation and hyperphosphorylation of tau-proteins is also tightly associated with protective mechanisms of cells and with processes of evacuation of phosphates, adenosine monophosphates and pyrophosphates from the region of protein synthesis. Prolonged highly intensive protein synthesis causes overload of protective mechanisms and impairments in concerted metabolic processes. This leads to neuronal dysfunction, transport collapse, and death of neurons. triggering factors (dpeaa)DE-He213 β-amyloid (dpeaa)DE-He213 Alzheimer’s disease (dpeaa)DE-He213 amyloid precursor protein (dpeaa)DE-He213 neuronal death (dpeaa)DE-He213 protein synthesis (dpeaa)DE-He213 tau-protein (dpeaa)DE-He213 phosphorylation (dpeaa)DE-He213 Dovidchenko, N. V. aut Uteshev, V. K. aut Sokolik, V. V. aut Shtang, O. M. aut Yakushin, M. A. aut Sokolova, N. M. aut Surin, A. K. aut Galzitskaya, O. V. aut Enthalten in Biochemistry (Moscow) Dordrecht [u.a.] : Springer Science + Business Media B.V, 2007 7(2013), 4 vom: Okt., Seite 278-293 (DE-627)547662793 (DE-600)2391886-X 1990-7516 nnns volume:7 year:2013 number:4 month:10 pages:278-293 https://dx.doi.org/10.1134/S1990750813040057 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_65 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_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 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 AR 7 2013 4 10 278-293 |
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10.1134/S1990750813040057 doi (DE-627)SPR022600396 (SPR)S1990750813040057-e DE-627 ger DE-627 rakwb eng Maltsev, A. V. verfasserin aut Intensive protein synthesis in neurons and phosphorylation of beta-amyloid precursor protein and tau-protein are triggering factors of neuronal amyloidosis and Alzheimer’s disease 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Pleiades Publishing, Ltd. 2013 Abstract Studies of Alzheimer’s disease have become particularly important and attract now much attention of scientists all over the world due to worldwide dissemination of this dangerous disorder. Causes of this pathology still remain unknown, while the final image, originally obtained on microscopic brain sections from patients with this disease more than a hundred years ago, is well familiar to clinicians. This includes deposition of amyloid-β (Aβ) in the brain tissue of senile plaques and fibrils. Many authors believe that the deposition of Aβ provokes secondary neuronal changes, responsible for death of neurons. Other authors associate the death of neurons with hyperphosphorylation of tau-proteins, which form neurofibrillar tangles inside nerve cells and cause their death. Creation of methods of preclinical diagnostics and effective treatment of Alzheimer’s disease requires novel knowledge: on the nature of triggering factors of sporadic forms of Alzheimer’s disease, on cause-effect relationships of phosphorylation of amyloid precursor protein with formation of pathogenic beta-amyloids, on the relationship between these factors underlying tau-protein hyperphosphorylation and neuron death. In this review we have analyzed reports describing increased intensity of protein synthesis in neurons under normal and various stress conditions, possibility of development of energy imbalance of neurons and activation of their protective systems. Phosphorylation and hyperphosphorylation of tau-proteins is also tightly associated with protective mechanisms of cells and with processes of evacuation of phosphates, adenosine monophosphates and pyrophosphates from the region of protein synthesis. Prolonged highly intensive protein synthesis causes overload of protective mechanisms and impairments in concerted metabolic processes. This leads to neuronal dysfunction, transport collapse, and death of neurons. triggering factors (dpeaa)DE-He213 β-amyloid (dpeaa)DE-He213 Alzheimer’s disease (dpeaa)DE-He213 amyloid precursor protein (dpeaa)DE-He213 neuronal death (dpeaa)DE-He213 protein synthesis (dpeaa)DE-He213 tau-protein (dpeaa)DE-He213 phosphorylation (dpeaa)DE-He213 Dovidchenko, N. V. aut Uteshev, V. K. aut Sokolik, V. V. aut Shtang, O. M. aut Yakushin, M. A. aut Sokolova, N. M. aut Surin, A. K. aut Galzitskaya, O. V. aut Enthalten in Biochemistry (Moscow) Dordrecht [u.a.] : Springer Science + Business Media B.V, 2007 7(2013), 4 vom: Okt., Seite 278-293 (DE-627)547662793 (DE-600)2391886-X 1990-7516 nnns volume:7 year:2013 number:4 month:10 pages:278-293 https://dx.doi.org/10.1134/S1990750813040057 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_65 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_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 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 AR 7 2013 4 10 278-293 |
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10.1134/S1990750813040057 doi (DE-627)SPR022600396 (SPR)S1990750813040057-e DE-627 ger DE-627 rakwb eng Maltsev, A. V. verfasserin aut Intensive protein synthesis in neurons and phosphorylation of beta-amyloid precursor protein and tau-protein are triggering factors of neuronal amyloidosis and Alzheimer’s disease 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Pleiades Publishing, Ltd. 2013 Abstract Studies of Alzheimer’s disease have become particularly important and attract now much attention of scientists all over the world due to worldwide dissemination of this dangerous disorder. Causes of this pathology still remain unknown, while the final image, originally obtained on microscopic brain sections from patients with this disease more than a hundred years ago, is well familiar to clinicians. This includes deposition of amyloid-β (Aβ) in the brain tissue of senile plaques and fibrils. Many authors believe that the deposition of Aβ provokes secondary neuronal changes, responsible for death of neurons. Other authors associate the death of neurons with hyperphosphorylation of tau-proteins, which form neurofibrillar tangles inside nerve cells and cause their death. Creation of methods of preclinical diagnostics and effective treatment of Alzheimer’s disease requires novel knowledge: on the nature of triggering factors of sporadic forms of Alzheimer’s disease, on cause-effect relationships of phosphorylation of amyloid precursor protein with formation of pathogenic beta-amyloids, on the relationship between these factors underlying tau-protein hyperphosphorylation and neuron death. In this review we have analyzed reports describing increased intensity of protein synthesis in neurons under normal and various stress conditions, possibility of development of energy imbalance of neurons and activation of their protective systems. Phosphorylation and hyperphosphorylation of tau-proteins is also tightly associated with protective mechanisms of cells and with processes of evacuation of phosphates, adenosine monophosphates and pyrophosphates from the region of protein synthesis. Prolonged highly intensive protein synthesis causes overload of protective mechanisms and impairments in concerted metabolic processes. This leads to neuronal dysfunction, transport collapse, and death of neurons. triggering factors (dpeaa)DE-He213 β-amyloid (dpeaa)DE-He213 Alzheimer’s disease (dpeaa)DE-He213 amyloid precursor protein (dpeaa)DE-He213 neuronal death (dpeaa)DE-He213 protein synthesis (dpeaa)DE-He213 tau-protein (dpeaa)DE-He213 phosphorylation (dpeaa)DE-He213 Dovidchenko, N. V. aut Uteshev, V. K. aut Sokolik, V. V. aut Shtang, O. M. aut Yakushin, M. A. aut Sokolova, N. M. aut Surin, A. K. aut Galzitskaya, O. V. aut Enthalten in Biochemistry (Moscow) Dordrecht [u.a.] : Springer Science + Business Media B.V, 2007 7(2013), 4 vom: Okt., Seite 278-293 (DE-627)547662793 (DE-600)2391886-X 1990-7516 nnns volume:7 year:2013 number:4 month:10 pages:278-293 https://dx.doi.org/10.1134/S1990750813040057 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_65 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_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 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 AR 7 2013 4 10 278-293 |
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10.1134/S1990750813040057 doi (DE-627)SPR022600396 (SPR)S1990750813040057-e DE-627 ger DE-627 rakwb eng Maltsev, A. V. verfasserin aut Intensive protein synthesis in neurons and phosphorylation of beta-amyloid precursor protein and tau-protein are triggering factors of neuronal amyloidosis and Alzheimer’s disease 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Pleiades Publishing, Ltd. 2013 Abstract Studies of Alzheimer’s disease have become particularly important and attract now much attention of scientists all over the world due to worldwide dissemination of this dangerous disorder. Causes of this pathology still remain unknown, while the final image, originally obtained on microscopic brain sections from patients with this disease more than a hundred years ago, is well familiar to clinicians. This includes deposition of amyloid-β (Aβ) in the brain tissue of senile plaques and fibrils. Many authors believe that the deposition of Aβ provokes secondary neuronal changes, responsible for death of neurons. Other authors associate the death of neurons with hyperphosphorylation of tau-proteins, which form neurofibrillar tangles inside nerve cells and cause their death. Creation of methods of preclinical diagnostics and effective treatment of Alzheimer’s disease requires novel knowledge: on the nature of triggering factors of sporadic forms of Alzheimer’s disease, on cause-effect relationships of phosphorylation of amyloid precursor protein with formation of pathogenic beta-amyloids, on the relationship between these factors underlying tau-protein hyperphosphorylation and neuron death. In this review we have analyzed reports describing increased intensity of protein synthesis in neurons under normal and various stress conditions, possibility of development of energy imbalance of neurons and activation of their protective systems. Phosphorylation and hyperphosphorylation of tau-proteins is also tightly associated with protective mechanisms of cells and with processes of evacuation of phosphates, adenosine monophosphates and pyrophosphates from the region of protein synthesis. Prolonged highly intensive protein synthesis causes overload of protective mechanisms and impairments in concerted metabolic processes. This leads to neuronal dysfunction, transport collapse, and death of neurons. triggering factors (dpeaa)DE-He213 β-amyloid (dpeaa)DE-He213 Alzheimer’s disease (dpeaa)DE-He213 amyloid precursor protein (dpeaa)DE-He213 neuronal death (dpeaa)DE-He213 protein synthesis (dpeaa)DE-He213 tau-protein (dpeaa)DE-He213 phosphorylation (dpeaa)DE-He213 Dovidchenko, N. V. aut Uteshev, V. K. aut Sokolik, V. V. aut Shtang, O. M. aut Yakushin, M. A. aut Sokolova, N. M. aut Surin, A. K. aut Galzitskaya, O. V. aut Enthalten in Biochemistry (Moscow) Dordrecht [u.a.] : Springer Science + Business Media B.V, 2007 7(2013), 4 vom: Okt., Seite 278-293 (DE-627)547662793 (DE-600)2391886-X 1990-7516 nnns volume:7 year:2013 number:4 month:10 pages:278-293 https://dx.doi.org/10.1134/S1990750813040057 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_65 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_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 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 AR 7 2013 4 10 278-293 |
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10.1134/S1990750813040057 doi (DE-627)SPR022600396 (SPR)S1990750813040057-e DE-627 ger DE-627 rakwb eng Maltsev, A. V. verfasserin aut Intensive protein synthesis in neurons and phosphorylation of beta-amyloid precursor protein and tau-protein are triggering factors of neuronal amyloidosis and Alzheimer’s disease 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Pleiades Publishing, Ltd. 2013 Abstract Studies of Alzheimer’s disease have become particularly important and attract now much attention of scientists all over the world due to worldwide dissemination of this dangerous disorder. Causes of this pathology still remain unknown, while the final image, originally obtained on microscopic brain sections from patients with this disease more than a hundred years ago, is well familiar to clinicians. This includes deposition of amyloid-β (Aβ) in the brain tissue of senile plaques and fibrils. Many authors believe that the deposition of Aβ provokes secondary neuronal changes, responsible for death of neurons. Other authors associate the death of neurons with hyperphosphorylation of tau-proteins, which form neurofibrillar tangles inside nerve cells and cause their death. Creation of methods of preclinical diagnostics and effective treatment of Alzheimer’s disease requires novel knowledge: on the nature of triggering factors of sporadic forms of Alzheimer’s disease, on cause-effect relationships of phosphorylation of amyloid precursor protein with formation of pathogenic beta-amyloids, on the relationship between these factors underlying tau-protein hyperphosphorylation and neuron death. In this review we have analyzed reports describing increased intensity of protein synthesis in neurons under normal and various stress conditions, possibility of development of energy imbalance of neurons and activation of their protective systems. Phosphorylation and hyperphosphorylation of tau-proteins is also tightly associated with protective mechanisms of cells and with processes of evacuation of phosphates, adenosine monophosphates and pyrophosphates from the region of protein synthesis. Prolonged highly intensive protein synthesis causes overload of protective mechanisms and impairments in concerted metabolic processes. This leads to neuronal dysfunction, transport collapse, and death of neurons. triggering factors (dpeaa)DE-He213 β-amyloid (dpeaa)DE-He213 Alzheimer’s disease (dpeaa)DE-He213 amyloid precursor protein (dpeaa)DE-He213 neuronal death (dpeaa)DE-He213 protein synthesis (dpeaa)DE-He213 tau-protein (dpeaa)DE-He213 phosphorylation (dpeaa)DE-He213 Dovidchenko, N. V. aut Uteshev, V. K. aut Sokolik, V. V. aut Shtang, O. M. aut Yakushin, M. A. aut Sokolova, N. M. aut Surin, A. K. aut Galzitskaya, O. V. aut Enthalten in Biochemistry (Moscow) Dordrecht [u.a.] : Springer Science + Business Media B.V, 2007 7(2013), 4 vom: Okt., Seite 278-293 (DE-627)547662793 (DE-600)2391886-X 1990-7516 nnns volume:7 year:2013 number:4 month:10 pages:278-293 https://dx.doi.org/10.1134/S1990750813040057 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_65 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_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 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 AR 7 2013 4 10 278-293 |
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Enthalten in Biochemistry (Moscow) 7(2013), 4 vom: Okt., Seite 278-293 volume:7 year:2013 number:4 month:10 pages:278-293 |
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Enthalten in Biochemistry (Moscow) 7(2013), 4 vom: Okt., Seite 278-293 volume:7 year:2013 number:4 month:10 pages:278-293 |
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Maltsev, A. V. @@aut@@ Dovidchenko, N. V. @@aut@@ Uteshev, V. K. @@aut@@ Sokolik, V. V. @@aut@@ Shtang, O. M. @@aut@@ Yakushin, M. A. @@aut@@ Sokolova, N. M. @@aut@@ Surin, A. K. @@aut@@ Galzitskaya, O. V. @@aut@@ |
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V.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Intensive protein synthesis in neurons and phosphorylation of beta-amyloid precursor protein and tau-protein are triggering factors of neuronal amyloidosis and Alzheimer’s disease</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2013</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="500" ind1=" " ind2=" "><subfield code="a">© Pleiades Publishing, Ltd. 2013</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract Studies of Alzheimer’s disease have become particularly important and attract now much attention of scientists all over the world due to worldwide dissemination of this dangerous disorder. Causes of this pathology still remain unknown, while the final image, originally obtained on microscopic brain sections from patients with this disease more than a hundred years ago, is well familiar to clinicians. This includes deposition of amyloid-β (Aβ) in the brain tissue of senile plaques and fibrils. Many authors believe that the deposition of Aβ provokes secondary neuronal changes, responsible for death of neurons. Other authors associate the death of neurons with hyperphosphorylation of tau-proteins, which form neurofibrillar tangles inside nerve cells and cause their death. Creation of methods of preclinical diagnostics and effective treatment of Alzheimer’s disease requires novel knowledge: on the nature of triggering factors of sporadic forms of Alzheimer’s disease, on cause-effect relationships of phosphorylation of amyloid precursor protein with formation of pathogenic beta-amyloids, on the relationship between these factors underlying tau-protein hyperphosphorylation and neuron death. In this review we have analyzed reports describing increased intensity of protein synthesis in neurons under normal and various stress conditions, possibility of development of energy imbalance of neurons and activation of their protective systems. Phosphorylation and hyperphosphorylation of tau-proteins is also tightly associated with protective mechanisms of cells and with processes of evacuation of phosphates, adenosine monophosphates and pyrophosphates from the region of protein synthesis. Prolonged highly intensive protein synthesis causes overload of protective mechanisms and impairments in concerted metabolic processes. 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Maltsev, A. V. |
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Maltsev, A. V. misc triggering factors misc β-amyloid misc Alzheimer’s disease misc amyloid precursor protein misc neuronal death misc protein synthesis misc tau-protein misc phosphorylation Intensive protein synthesis in neurons and phosphorylation of beta-amyloid precursor protein and tau-protein are triggering factors of neuronal amyloidosis and Alzheimer’s disease |
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Intensive protein synthesis in neurons and phosphorylation of beta-amyloid precursor protein and tau-protein are triggering factors of neuronal amyloidosis and Alzheimer’s disease triggering factors (dpeaa)DE-He213 β-amyloid (dpeaa)DE-He213 Alzheimer’s disease (dpeaa)DE-He213 amyloid precursor protein (dpeaa)DE-He213 neuronal death (dpeaa)DE-He213 protein synthesis (dpeaa)DE-He213 tau-protein (dpeaa)DE-He213 phosphorylation (dpeaa)DE-He213 |
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Intensive protein synthesis in neurons and phosphorylation of beta-amyloid precursor protein and tau-protein are triggering factors of neuronal amyloidosis and Alzheimer’s disease |
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Maltsev, A. V. Dovidchenko, N. V. Uteshev, V. K. Sokolik, V. V. Shtang, O. M. Yakushin, M. A. Sokolova, N. M. Surin, A. K. Galzitskaya, O. V. |
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Elektronische Aufsätze |
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Maltsev, A. V. |
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10.1134/S1990750813040057 |
| title_sort |
intensive protein synthesis in neurons and phosphorylation of beta-amyloid precursor protein and tau-protein are triggering factors of neuronal amyloidosis and alzheimer’s disease |
| title_auth |
Intensive protein synthesis in neurons and phosphorylation of beta-amyloid precursor protein and tau-protein are triggering factors of neuronal amyloidosis and Alzheimer’s disease |
| abstract |
Abstract Studies of Alzheimer’s disease have become particularly important and attract now much attention of scientists all over the world due to worldwide dissemination of this dangerous disorder. Causes of this pathology still remain unknown, while the final image, originally obtained on microscopic brain sections from patients with this disease more than a hundred years ago, is well familiar to clinicians. This includes deposition of amyloid-β (Aβ) in the brain tissue of senile plaques and fibrils. Many authors believe that the deposition of Aβ provokes secondary neuronal changes, responsible for death of neurons. Other authors associate the death of neurons with hyperphosphorylation of tau-proteins, which form neurofibrillar tangles inside nerve cells and cause their death. Creation of methods of preclinical diagnostics and effective treatment of Alzheimer’s disease requires novel knowledge: on the nature of triggering factors of sporadic forms of Alzheimer’s disease, on cause-effect relationships of phosphorylation of amyloid precursor protein with formation of pathogenic beta-amyloids, on the relationship between these factors underlying tau-protein hyperphosphorylation and neuron death. In this review we have analyzed reports describing increased intensity of protein synthesis in neurons under normal and various stress conditions, possibility of development of energy imbalance of neurons and activation of their protective systems. Phosphorylation and hyperphosphorylation of tau-proteins is also tightly associated with protective mechanisms of cells and with processes of evacuation of phosphates, adenosine monophosphates and pyrophosphates from the region of protein synthesis. Prolonged highly intensive protein synthesis causes overload of protective mechanisms and impairments in concerted metabolic processes. This leads to neuronal dysfunction, transport collapse, and death of neurons. © Pleiades Publishing, Ltd. 2013 |
| abstractGer |
Abstract Studies of Alzheimer’s disease have become particularly important and attract now much attention of scientists all over the world due to worldwide dissemination of this dangerous disorder. Causes of this pathology still remain unknown, while the final image, originally obtained on microscopic brain sections from patients with this disease more than a hundred years ago, is well familiar to clinicians. This includes deposition of amyloid-β (Aβ) in the brain tissue of senile plaques and fibrils. Many authors believe that the deposition of Aβ provokes secondary neuronal changes, responsible for death of neurons. Other authors associate the death of neurons with hyperphosphorylation of tau-proteins, which form neurofibrillar tangles inside nerve cells and cause their death. Creation of methods of preclinical diagnostics and effective treatment of Alzheimer’s disease requires novel knowledge: on the nature of triggering factors of sporadic forms of Alzheimer’s disease, on cause-effect relationships of phosphorylation of amyloid precursor protein with formation of pathogenic beta-amyloids, on the relationship between these factors underlying tau-protein hyperphosphorylation and neuron death. In this review we have analyzed reports describing increased intensity of protein synthesis in neurons under normal and various stress conditions, possibility of development of energy imbalance of neurons and activation of their protective systems. Phosphorylation and hyperphosphorylation of tau-proteins is also tightly associated with protective mechanisms of cells and with processes of evacuation of phosphates, adenosine monophosphates and pyrophosphates from the region of protein synthesis. Prolonged highly intensive protein synthesis causes overload of protective mechanisms and impairments in concerted metabolic processes. This leads to neuronal dysfunction, transport collapse, and death of neurons. © Pleiades Publishing, Ltd. 2013 |
| abstract_unstemmed |
Abstract Studies of Alzheimer’s disease have become particularly important and attract now much attention of scientists all over the world due to worldwide dissemination of this dangerous disorder. Causes of this pathology still remain unknown, while the final image, originally obtained on microscopic brain sections from patients with this disease more than a hundred years ago, is well familiar to clinicians. This includes deposition of amyloid-β (Aβ) in the brain tissue of senile plaques and fibrils. Many authors believe that the deposition of Aβ provokes secondary neuronal changes, responsible for death of neurons. Other authors associate the death of neurons with hyperphosphorylation of tau-proteins, which form neurofibrillar tangles inside nerve cells and cause their death. Creation of methods of preclinical diagnostics and effective treatment of Alzheimer’s disease requires novel knowledge: on the nature of triggering factors of sporadic forms of Alzheimer’s disease, on cause-effect relationships of phosphorylation of amyloid precursor protein with formation of pathogenic beta-amyloids, on the relationship between these factors underlying tau-protein hyperphosphorylation and neuron death. In this review we have analyzed reports describing increased intensity of protein synthesis in neurons under normal and various stress conditions, possibility of development of energy imbalance of neurons and activation of their protective systems. Phosphorylation and hyperphosphorylation of tau-proteins is also tightly associated with protective mechanisms of cells and with processes of evacuation of phosphates, adenosine monophosphates and pyrophosphates from the region of protein synthesis. Prolonged highly intensive protein synthesis causes overload of protective mechanisms and impairments in concerted metabolic processes. This leads to neuronal dysfunction, transport collapse, and death of neurons. © Pleiades Publishing, Ltd. 2013 |
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Intensive protein synthesis in neurons and phosphorylation of beta-amyloid precursor protein and tau-protein are triggering factors of neuronal amyloidosis and Alzheimer’s disease |
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| score |
7.4011803 |