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- W92763239 abstract "Polymerization of amyloid β-peptide (Aβ) results in neuronal toxicity in vitro, and the formation in vivo of Aβ-peptide plaque is associated with the onset and progression of Alzheimer’s disease (AD) (Lorenzo and Yankner, 1994 and references therein). The precise mechanism by which AD-associated cellular toxicity and neurodegeneration occurs in humans is incompletely understood. Recent identification of the specific genetic defects that result in four classes of familial AD have the common feature of enhancing the production or deposition of Aβ (Scikoe, 1997). These data, in combination with additional observations regarding the progression of AD in Down syndrome patients or sporadic AD in older patients, the neurological and behavioral pathology of transgenic animal models of AD, and various biochemical properties of Aβ point to the production and subsequent polymerization of Aβ as an essential component of AD pathogenesis. This “Amyloid Hyposthesis” is reviewed in greater detail in the chapter by M. S. Shearman (see above). Thus, identification of compounds that slow, prevent, and possibly reverse the polymerization of Aβ has emerged as a goal in the development of therapeutic agents for AD.KeywordsDown SyndromeFibril FormationIslet Amyloid PolypeptideSpecific Genetic DefectPolymerization AssayThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves." @default.
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- W92763239 date "1998-01-01" @default.
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- W92763239 title "Discovery and Characterization of Peptidoorganic Inhibitors of Amyloid β-Peptide Polymerization" @default.
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