Abstract
Amyloid-βpeptide (Aβ) is the major component of senile plaques deposited in the brains of patients with Alzheimer disease (AD). Several lines of evidence suggest that the accumulation of A βis linked to the pathogenesis of AD. A βis derived from amyloid-βprecursor protein (APP) that is sequentially cleaved by two aspartate proteases, β- and γ- secretases. Advances in basic research and observational study implicate that that drugs that inhibit or modulate the proteolytic activity of these secretases could provide a disease- modifying therapy against AD as pre- emptive medicine. In addition, evolutional genome sequencing technologies reveal several genetic risk factors, which may impact on the onset of AD. In this review, I will discuss about recent status regarding the development of therapeutics for AD.
