Preventing β-amyloid fibrillization and deposition: β-sheet breakers and pathological chaperone inhibitors
<p>Abstract</p> <p>Central to the pathogenesis of Alzheimer's disease (AD) is the conversion of normal, soluble β-amyloid (sAβ) to oligomeric, fibrillar Aβ. This process of conformational conversion can be influenced by interactions with other proteins that can stabilize the d...
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Format: | Article |
Language: | English |
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BMC
2008-12-01
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Series: | BMC Neuroscience |
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author | Wisniewski Thomas Sadowski Martin |
author_facet | Wisniewski Thomas Sadowski Martin |
author_sort | Wisniewski Thomas |
collection | DOAJ |
description | <p>Abstract</p> <p>Central to the pathogenesis of Alzheimer's disease (AD) is the conversion of normal, soluble β-amyloid (sAβ) to oligomeric, fibrillar Aβ. This process of conformational conversion can be influenced by interactions with other proteins that can stabilize the disease-associated state; these proteins have been termed 'pathological chaperones'. In a number of AD models, intervention that block soluble Aβ aggregation, including β-sheet breakers, and compounds that block interactions with pathological chaperones, have been shown to be highly effective. When combined with early pathology detection, these therapeutic strategies hold great promise as effective and relatively toxicity free methods of preventing AD related pathology.</p> |
first_indexed | 2024-04-14T04:17:41Z |
format | Article |
id | doaj.art-aef0506f86ba4f31ac3b7f2424274430 |
institution | Directory Open Access Journal |
issn | 1471-2202 |
language | English |
last_indexed | 2024-04-14T04:17:41Z |
publishDate | 2008-12-01 |
publisher | BMC |
record_format | Article |
series | BMC Neuroscience |
spelling | doaj.art-aef0506f86ba4f31ac3b7f24242744302022-12-22T02:12:42ZengBMCBMC Neuroscience1471-22022008-12-019Suppl 2S510.1186/1471-2202-9-S2-S5Preventing β-amyloid fibrillization and deposition: β-sheet breakers and pathological chaperone inhibitorsWisniewski ThomasSadowski Martin<p>Abstract</p> <p>Central to the pathogenesis of Alzheimer's disease (AD) is the conversion of normal, soluble β-amyloid (sAβ) to oligomeric, fibrillar Aβ. This process of conformational conversion can be influenced by interactions with other proteins that can stabilize the disease-associated state; these proteins have been termed 'pathological chaperones'. In a number of AD models, intervention that block soluble Aβ aggregation, including β-sheet breakers, and compounds that block interactions with pathological chaperones, have been shown to be highly effective. When combined with early pathology detection, these therapeutic strategies hold great promise as effective and relatively toxicity free methods of preventing AD related pathology.</p> |
spellingShingle | Wisniewski Thomas Sadowski Martin Preventing β-amyloid fibrillization and deposition: β-sheet breakers and pathological chaperone inhibitors BMC Neuroscience |
title | Preventing β-amyloid fibrillization and deposition: β-sheet breakers and pathological chaperone inhibitors |
title_full | Preventing β-amyloid fibrillization and deposition: β-sheet breakers and pathological chaperone inhibitors |
title_fullStr | Preventing β-amyloid fibrillization and deposition: β-sheet breakers and pathological chaperone inhibitors |
title_full_unstemmed | Preventing β-amyloid fibrillization and deposition: β-sheet breakers and pathological chaperone inhibitors |
title_short | Preventing β-amyloid fibrillization and deposition: β-sheet breakers and pathological chaperone inhibitors |
title_sort | preventing β amyloid fibrillization and deposition β sheet breakers and pathological chaperone inhibitors |
work_keys_str_mv | AT wisniewskithomas preventingbamyloidfibrillizationanddepositionbsheetbreakersandpathologicalchaperoneinhibitors AT sadowskimartin preventingbamyloidfibrillizationanddepositionbsheetbreakersandpathologicalchaperoneinhibitors |