Small molecule inhibitors of Aβ‐aggregation and neurotoxicity

Abstract

Abstract Alzheimer disease (AD) is characterized pathologically by extracellular amyloid deposits composed of Aβ peptide, neurofibrillary tangles (NFTs) made up of hyperphosphorylated tau, and a deficit of cholinergic neurons in the basal forebrain. Presently, only symptomatic therapies are available for the treatment of AD and these therapies have a limited time frame of utility. Amyloid disorders represent the effects of chronic Aβ production and are not a secondary pathological effect caused by a distant trigger; therefore targeting Aβ is a viable pursuit. In this review, we will discuss the various small molecule anti‐aggregation inhibitors that have been reported in the literature, with emphasis on compounds that are presently being investigated in clinical trials. Drug Dev Res 70, 2009. © 2009 Wiley‐Liss, Inc.