Affiliations: Drexel University College of Medicine, Department of Neurobiology and Anatomy, Philadelphia, PA, USA
Correspondence:
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Correspondence to: Christopher Haas, Drexel University College of Medicine, Department of Neurobiology and Anatomy, 2900 West Queen Lane, Philadelphia, PA 19129, USA. Tel.: +1 (215) 991 8459; Fax: +1 (215) 843 9082; E-mail: cjh62@drexel.edu.
Abstract: Therapeutic options for Alzheimer's disease are currently limited to symptomatic treatment that only provides modest and temporary maintenance of cognitive and memory functions, without altering disease progression. Although a variety of therapeutics targeting amyloid production or plaque degradation as well as tau hyperphosphorylation and aggregation have been proposed, examined in pre-clinical models and introduced into clinical trials, many have failed to provide significant therapeutic benefit. Concerns over the adequacy of currently used pre-clinical models, in addition to questions pertaining to the timing of therapeutic administration, vis-à-vis synaptic and neuronal loss have been raised, and are further complicated by the genetic diversity of individual patients. This review will provide a brief overview of Alzheimer's disease pathophysiology and the currently approved therapeutics, while the main section will focus on therapeutics currently evaluated in pre-clinical models and clinical trials.
Keywords: Alzheimer's disease, amyloid-β, drug therapy, humans, investigational drugs, pathophysiology, tau
