Neuritic plaques composed of amyloid β-protein (Aβ) are an early and invariant neuropathological feature of Alzheimer's disease (AD). The current preclinical search for drugs is mainly focused on decreasing Aβ production by inhibiting β- or γ-secretase, blocking the formation of these plaques by preventing Aβ protofibril and fibril formation, and alleviating the toxic effects of neuritic plaque deposition. Increasing numbers of drugs currently used as therapies for other diseases are now entering clinical trials for AD, but the molecular targets of these drugs and their relevance to Aβ toxicity needs to be thoroughly addressed. This knowledge will allow us to fully understand the Aβ-related pathways in AD pathogenesis and explore novel therapeutic interventions.
|Original language||English (US)|
|Number of pages||5|
|Journal||Current Opinion in Investigational Drugs|
|State||Published - Jan 1 2003|
ASJC Scopus subject areas