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...

Full description

Bibliographic Details
Main Authors: Wisniewski Thomas, Sadowski Martin
Format: Article
Language:English
Published: BMC 2008-12-01
Series:BMC Neuroscience
_version_ 1818473124462592000
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