Molecular dynamics of amyloid β-protein aggregation

抄録

Alzheimer’s disease (AD) is a common cause of dementia, characterized by progressive memory loss and various functional impairments in the brain. Amyloid β-proteins (Aβ) is a main component of senile plaques, which is a major pathological features of AD. According to the amyloid cascade hypothesis, the deposition of Aβ in the brain is a key stone of the pathogenesis of AD. During the past decade, several Aβ-targetted medications have been developed, and the clinical trials for AD have been performed so far. In this article, we summarize the clinical features of AD and the molecular mechanisms of Aβ. In addition, we focus a content about the transmissible potencies of Aβ pathology and the inactivation methods against Aβ aggregates to prevent the transmission of Aβ among individuals.