Anti-Amyloid Drugs
Summary The requirements for amyloidogenesis, as it is currently understood, include an adequate amyloid precursor pool, a nidus for fibrillogenesis, interactions with a set of common components (most of which are involved in basement membrane structure) and amyloid turnover. These factors serve as...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Kisilevsky, Robert [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
1996 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Drugs & aging - Berlin [u.a.] : Springer, 1991, 8(1996), 2 vom: Feb., Seite 75-83 |
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| Übergeordnetes Werk: |
volume:8 ; year:1996 ; number:2 ; month:02 ; pages:75-83 |
| Links: |
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| DOI / URN: |
10.2165/00002512-199608020-00001 |
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SPR033228329 |
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| 520 | |a Summary The requirements for amyloidogenesis, as it is currently understood, include an adequate amyloid precursor pool, a nidus for fibrillogenesis, interactions with a set of common components (most of which are involved in basement membrane structure) and amyloid turnover. These factors serve as the basis for therapeutic attack. General strategies focusing on each of these factors are presented with examples from the experimental and clinical literature. These include reducing the amyloid precursor protein pool in familial amyloid polyneuropathy by liver transplantation, inhibiting nidus formation in familial Mediterranean fever by the use of colchicine, inhibiting amyloid precursor protein/heparan sulphate interaction in experimental inflammation-associated amyloidosis by the use of novel small molecule anionic sulphates and sulphonates, and the use of new analogues of doxorubicin in light chain amyloidosis to accelerate amyloid removal. The potential significance of local and systemic amyloid deposits is discussed in the light of new information on the genetics of Alzheimer’s disease, observations made in patients receiving long term dialysis for renal failure, and the potential involvement of amyloid deposits in the pathogenesis of non—insulin-dependent diabetes mellitus. | ||
| 650 | 4 | |a Amyloidosis |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Familial Mediterranean Fever |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Amyloid Deposition |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Amyloid Fibril |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Ethionine |7 (dpeaa)DE-He213 | |
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10.2165/00002512-199608020-00001 doi (DE-627)SPR033228329 (SPR)00002512-199608020-00001-e DE-627 ger DE-627 rakwb eng 610 ASE Kisilevsky, Robert verfasserin aut Anti-Amyloid Drugs 1996 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary The requirements for amyloidogenesis, as it is currently understood, include an adequate amyloid precursor pool, a nidus for fibrillogenesis, interactions with a set of common components (most of which are involved in basement membrane structure) and amyloid turnover. These factors serve as the basis for therapeutic attack. General strategies focusing on each of these factors are presented with examples from the experimental and clinical literature. These include reducing the amyloid precursor protein pool in familial amyloid polyneuropathy by liver transplantation, inhibiting nidus formation in familial Mediterranean fever by the use of colchicine, inhibiting amyloid precursor protein/heparan sulphate interaction in experimental inflammation-associated amyloidosis by the use of novel small molecule anionic sulphates and sulphonates, and the use of new analogues of doxorubicin in light chain amyloidosis to accelerate amyloid removal. The potential significance of local and systemic amyloid deposits is discussed in the light of new information on the genetics of Alzheimer’s disease, observations made in patients receiving long term dialysis for renal failure, and the potential involvement of amyloid deposits in the pathogenesis of non—insulin-dependent diabetes mellitus. Amyloidosis (dpeaa)DE-He213 Familial Mediterranean Fever (dpeaa)DE-He213 Amyloid Deposition (dpeaa)DE-He213 Amyloid Fibril (dpeaa)DE-He213 Ethionine (dpeaa)DE-He213 Enthalten in Drugs & aging Berlin [u.a.] : Springer, 1991 8(1996), 2 vom: Feb., Seite 75-83 (DE-627)327644281 (DE-600)2043689-0 1179-1969 nnns volume:8 year:1996 number:2 month:02 pages:75-83 https://dx.doi.org/10.2165/00002512-199608020-00001 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA SSG-OPC-PHA SSG-OPC-ASE GBV_ILN_702 GBV_ILN_2190 AR 8 1996 2 02 75-83 |
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10.2165/00002512-199608020-00001 doi (DE-627)SPR033228329 (SPR)00002512-199608020-00001-e DE-627 ger DE-627 rakwb eng 610 ASE Kisilevsky, Robert verfasserin aut Anti-Amyloid Drugs 1996 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary The requirements for amyloidogenesis, as it is currently understood, include an adequate amyloid precursor pool, a nidus for fibrillogenesis, interactions with a set of common components (most of which are involved in basement membrane structure) and amyloid turnover. These factors serve as the basis for therapeutic attack. General strategies focusing on each of these factors are presented with examples from the experimental and clinical literature. These include reducing the amyloid precursor protein pool in familial amyloid polyneuropathy by liver transplantation, inhibiting nidus formation in familial Mediterranean fever by the use of colchicine, inhibiting amyloid precursor protein/heparan sulphate interaction in experimental inflammation-associated amyloidosis by the use of novel small molecule anionic sulphates and sulphonates, and the use of new analogues of doxorubicin in light chain amyloidosis to accelerate amyloid removal. The potential significance of local and systemic amyloid deposits is discussed in the light of new information on the genetics of Alzheimer’s disease, observations made in patients receiving long term dialysis for renal failure, and the potential involvement of amyloid deposits in the pathogenesis of non—insulin-dependent diabetes mellitus. Amyloidosis (dpeaa)DE-He213 Familial Mediterranean Fever (dpeaa)DE-He213 Amyloid Deposition (dpeaa)DE-He213 Amyloid Fibril (dpeaa)DE-He213 Ethionine (dpeaa)DE-He213 Enthalten in Drugs & aging Berlin [u.a.] : Springer, 1991 8(1996), 2 vom: Feb., Seite 75-83 (DE-627)327644281 (DE-600)2043689-0 1179-1969 nnns volume:8 year:1996 number:2 month:02 pages:75-83 https://dx.doi.org/10.2165/00002512-199608020-00001 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA SSG-OPC-PHA SSG-OPC-ASE GBV_ILN_702 GBV_ILN_2190 AR 8 1996 2 02 75-83 |
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10.2165/00002512-199608020-00001 doi (DE-627)SPR033228329 (SPR)00002512-199608020-00001-e DE-627 ger DE-627 rakwb eng 610 ASE Kisilevsky, Robert verfasserin aut Anti-Amyloid Drugs 1996 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary The requirements for amyloidogenesis, as it is currently understood, include an adequate amyloid precursor pool, a nidus for fibrillogenesis, interactions with a set of common components (most of which are involved in basement membrane structure) and amyloid turnover. These factors serve as the basis for therapeutic attack. General strategies focusing on each of these factors are presented with examples from the experimental and clinical literature. These include reducing the amyloid precursor protein pool in familial amyloid polyneuropathy by liver transplantation, inhibiting nidus formation in familial Mediterranean fever by the use of colchicine, inhibiting amyloid precursor protein/heparan sulphate interaction in experimental inflammation-associated amyloidosis by the use of novel small molecule anionic sulphates and sulphonates, and the use of new analogues of doxorubicin in light chain amyloidosis to accelerate amyloid removal. The potential significance of local and systemic amyloid deposits is discussed in the light of new information on the genetics of Alzheimer’s disease, observations made in patients receiving long term dialysis for renal failure, and the potential involvement of amyloid deposits in the pathogenesis of non—insulin-dependent diabetes mellitus. Amyloidosis (dpeaa)DE-He213 Familial Mediterranean Fever (dpeaa)DE-He213 Amyloid Deposition (dpeaa)DE-He213 Amyloid Fibril (dpeaa)DE-He213 Ethionine (dpeaa)DE-He213 Enthalten in Drugs & aging Berlin [u.a.] : Springer, 1991 8(1996), 2 vom: Feb., Seite 75-83 (DE-627)327644281 (DE-600)2043689-0 1179-1969 nnns volume:8 year:1996 number:2 month:02 pages:75-83 https://dx.doi.org/10.2165/00002512-199608020-00001 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA SSG-OPC-PHA SSG-OPC-ASE GBV_ILN_702 GBV_ILN_2190 AR 8 1996 2 02 75-83 |
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10.2165/00002512-199608020-00001 doi (DE-627)SPR033228329 (SPR)00002512-199608020-00001-e DE-627 ger DE-627 rakwb eng 610 ASE Kisilevsky, Robert verfasserin aut Anti-Amyloid Drugs 1996 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary The requirements for amyloidogenesis, as it is currently understood, include an adequate amyloid precursor pool, a nidus for fibrillogenesis, interactions with a set of common components (most of which are involved in basement membrane structure) and amyloid turnover. These factors serve as the basis for therapeutic attack. General strategies focusing on each of these factors are presented with examples from the experimental and clinical literature. These include reducing the amyloid precursor protein pool in familial amyloid polyneuropathy by liver transplantation, inhibiting nidus formation in familial Mediterranean fever by the use of colchicine, inhibiting amyloid precursor protein/heparan sulphate interaction in experimental inflammation-associated amyloidosis by the use of novel small molecule anionic sulphates and sulphonates, and the use of new analogues of doxorubicin in light chain amyloidosis to accelerate amyloid removal. The potential significance of local and systemic amyloid deposits is discussed in the light of new information on the genetics of Alzheimer’s disease, observations made in patients receiving long term dialysis for renal failure, and the potential involvement of amyloid deposits in the pathogenesis of non—insulin-dependent diabetes mellitus. Amyloidosis (dpeaa)DE-He213 Familial Mediterranean Fever (dpeaa)DE-He213 Amyloid Deposition (dpeaa)DE-He213 Amyloid Fibril (dpeaa)DE-He213 Ethionine (dpeaa)DE-He213 Enthalten in Drugs & aging Berlin [u.a.] : Springer, 1991 8(1996), 2 vom: Feb., Seite 75-83 (DE-627)327644281 (DE-600)2043689-0 1179-1969 nnns volume:8 year:1996 number:2 month:02 pages:75-83 https://dx.doi.org/10.2165/00002512-199608020-00001 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA SSG-OPC-PHA SSG-OPC-ASE GBV_ILN_702 GBV_ILN_2190 AR 8 1996 2 02 75-83 |
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10.2165/00002512-199608020-00001 doi (DE-627)SPR033228329 (SPR)00002512-199608020-00001-e DE-627 ger DE-627 rakwb eng 610 ASE Kisilevsky, Robert verfasserin aut Anti-Amyloid Drugs 1996 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary The requirements for amyloidogenesis, as it is currently understood, include an adequate amyloid precursor pool, a nidus for fibrillogenesis, interactions with a set of common components (most of which are involved in basement membrane structure) and amyloid turnover. These factors serve as the basis for therapeutic attack. General strategies focusing on each of these factors are presented with examples from the experimental and clinical literature. These include reducing the amyloid precursor protein pool in familial amyloid polyneuropathy by liver transplantation, inhibiting nidus formation in familial Mediterranean fever by the use of colchicine, inhibiting amyloid precursor protein/heparan sulphate interaction in experimental inflammation-associated amyloidosis by the use of novel small molecule anionic sulphates and sulphonates, and the use of new analogues of doxorubicin in light chain amyloidosis to accelerate amyloid removal. The potential significance of local and systemic amyloid deposits is discussed in the light of new information on the genetics of Alzheimer’s disease, observations made in patients receiving long term dialysis for renal failure, and the potential involvement of amyloid deposits in the pathogenesis of non—insulin-dependent diabetes mellitus. Amyloidosis (dpeaa)DE-He213 Familial Mediterranean Fever (dpeaa)DE-He213 Amyloid Deposition (dpeaa)DE-He213 Amyloid Fibril (dpeaa)DE-He213 Ethionine (dpeaa)DE-He213 Enthalten in Drugs & aging Berlin [u.a.] : Springer, 1991 8(1996), 2 vom: Feb., Seite 75-83 (DE-627)327644281 (DE-600)2043689-0 1179-1969 nnns volume:8 year:1996 number:2 month:02 pages:75-83 https://dx.doi.org/10.2165/00002512-199608020-00001 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA SSG-OPC-PHA SSG-OPC-ASE GBV_ILN_702 GBV_ILN_2190 AR 8 1996 2 02 75-83 |
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Summary The requirements for amyloidogenesis, as it is currently understood, include an adequate amyloid precursor pool, a nidus for fibrillogenesis, interactions with a set of common components (most of which are involved in basement membrane structure) and amyloid turnover. These factors serve as the basis for therapeutic attack. General strategies focusing on each of these factors are presented with examples from the experimental and clinical literature. These include reducing the amyloid precursor protein pool in familial amyloid polyneuropathy by liver transplantation, inhibiting nidus formation in familial Mediterranean fever by the use of colchicine, inhibiting amyloid precursor protein/heparan sulphate interaction in experimental inflammation-associated amyloidosis by the use of novel small molecule anionic sulphates and sulphonates, and the use of new analogues of doxorubicin in light chain amyloidosis to accelerate amyloid removal. The potential significance of local and systemic amyloid deposits is discussed in the light of new information on the genetics of Alzheimer’s disease, observations made in patients receiving long term dialysis for renal failure, and the potential involvement of amyloid deposits in the pathogenesis of non—insulin-dependent diabetes mellitus. |
| abstractGer |
Summary The requirements for amyloidogenesis, as it is currently understood, include an adequate amyloid precursor pool, a nidus for fibrillogenesis, interactions with a set of common components (most of which are involved in basement membrane structure) and amyloid turnover. These factors serve as the basis for therapeutic attack. General strategies focusing on each of these factors are presented with examples from the experimental and clinical literature. These include reducing the amyloid precursor protein pool in familial amyloid polyneuropathy by liver transplantation, inhibiting nidus formation in familial Mediterranean fever by the use of colchicine, inhibiting amyloid precursor protein/heparan sulphate interaction in experimental inflammation-associated amyloidosis by the use of novel small molecule anionic sulphates and sulphonates, and the use of new analogues of doxorubicin in light chain amyloidosis to accelerate amyloid removal. The potential significance of local and systemic amyloid deposits is discussed in the light of new information on the genetics of Alzheimer’s disease, observations made in patients receiving long term dialysis for renal failure, and the potential involvement of amyloid deposits in the pathogenesis of non—insulin-dependent diabetes mellitus. |
| abstract_unstemmed |
Summary The requirements for amyloidogenesis, as it is currently understood, include an adequate amyloid precursor pool, a nidus for fibrillogenesis, interactions with a set of common components (most of which are involved in basement membrane structure) and amyloid turnover. These factors serve as the basis for therapeutic attack. General strategies focusing on each of these factors are presented with examples from the experimental and clinical literature. These include reducing the amyloid precursor protein pool in familial amyloid polyneuropathy by liver transplantation, inhibiting nidus formation in familial Mediterranean fever by the use of colchicine, inhibiting amyloid precursor protein/heparan sulphate interaction in experimental inflammation-associated amyloidosis by the use of novel small molecule anionic sulphates and sulphonates, and the use of new analogues of doxorubicin in light chain amyloidosis to accelerate amyloid removal. The potential significance of local and systemic amyloid deposits is discussed in the light of new information on the genetics of Alzheimer’s disease, observations made in patients receiving long term dialysis for renal failure, and the potential involvement of amyloid deposits in the pathogenesis of non—insulin-dependent diabetes mellitus. |
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| title_short |
Anti-Amyloid Drugs |
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https://dx.doi.org/10.2165/00002512-199608020-00001 |
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10.2165/00002512-199608020-00001 |
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2024-07-03T17:25:46.555Z |
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