Alzheimer's disease (AD) is the most common cause of dementia, affecting tens of millions of individuals worldwide. Neuritic plaques are accumulations of aggregated amyloid beta (Aβ) peptides, including Aβ1-40 and Aβ1-42, derived from processing of amyloid precursor protein (APP) by β- and γ-secretases. The vast majority of autosomal familial AD (FAD)-linked mutations are associated with increased levels of Aβ1-42, providing strong evidence that Aβ1-42 plays a central role in AD pathogenesis. There are currently no effective therapies for arresting or reversing the impairment of cognitive function that characterizes AD. There is a need in the art for effective therapies for treating AD and related disorders.
Literature
Mueller-Steiner et al. (September 2006) Neuron 51:703-714; WO 2004/084830; Hook et al. (2005) Biol. Chem. 386:931-940; Hook (2006) BioDrugs 20:105-119; Hook (2006) Biol. Chem. 387:1429-1439; U.S. Patent Publication No. 2004/0248232; Cataldo and Nixon (1990) Proc. Natl. Acad. Sci. USA 87:3861-3865; Cataldo et al. (1997) J. Neurosci. 17:6142; Mackay et al. (1997) Eur. J. Biochem. 244:414-425.