Copy the page URI to the clipboard
Hawkes, Cheryl A.; Ng, Vivian and McLaurin, JoAnne
(2009).
DOI: https://doi.org/10.1002/ddr.20290
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.