Accumulation of β-amyloid protein (Aβ) in the brain is one of the key neuropathologic features of Alzheimer's disease. While current understanding of how Aβ is generated has grown there is still no approved treatment available that either prevents its formation or removes it from the brain. However, numerous treatment strategies are being tested that are aimed at each step of the amyloid pathway - from its initial liberation, to its early aggregation, and finally to the eventual formation of insoluble β-pleated sheets. Today, Aβ is the most accessible therapeutic target available for Alzheimer's disease. In the process of developing treatments based on Aβ modification, there is a great deal to learn not only about Alzheimer's disease but also about the normal function of the brain. This article discusses the current status of various strategies aimed at reducing amyloid burden in the brain.
|Original language||English (US)|
|Number of pages||5|
|State||Published - Jun 1 2009|
ASJC Scopus subject areas
- Psychiatry and Mental health