The Development of Preventives and Therapeutics for Alzheimers Disease that Inhibit the Formation of β-Amyloid Fibrils (fAβ), as Well as Destabilize Preformed fAβ

Title: The Development of Preventives and Therapeutics for Alzheimers Disease that Inhibit the Formation of β-Amyloid Fibrils (fAβ), as Well as Destabilize Preformed fAβ

Volume: 12 Issue: 33

Author(s): Kenjiro Ono, Hironobu Naiki and Masahito Yamada

Affiliation:

Keywords: Alzheimer's disease, β-amyloid fibrils, organic compounds, thioflavin T, electron microscopy

Abstract: Neuritic plaques composed mainly of amyloid β-protein (Aβ) in the brain are an early and invariant neuropathological feature of Alzheimers disease (AD). The current search for anti-AD drugs is mainly focused on modification of the process of Aβ deposition in the brain. In this article, the recent development of the molecules that inhibit the formation of β-amyloid fibrils (fAβ), as well as destabilize preformed fAβ is reviewed. Recently, various compounds such as curcumin, nicotine and wine-related polyphenols have been reported to inhibit the formation, extension of fAβ, as well as destabilize preformed fAβ at pH 7.5 at 37°C in vitro. In cell culture experiments, destabilized fAβ were suggested to be less toxic than intact fAβ. In transgenic mice model study, some coumpounds such as curcumin and nicotine have also been reported to reduce plaque burden in vivo. Although the mechanisms by which these compounds inhibit fAβ formation from Aβ, and destabilize preformed fAβ are still unclear, they could be key molecules for the development of preventives and therapeutics for AD.

Cite this article as:

Ono Kenjiro, Naiki Hironobu and Yamada Masahito, The Development of Preventives and Therapeutics for Alzheimers Disease that Inhibit the Formation of β-Amyloid Fibrils (fAβ), as Well as Destabilize Preformed fAβ, Current Pharmaceutical Design 2006; 12 (33) . https://dx.doi.org/10.2174/138161206778793010