CLINICAL TRIAL: PHASE 3 MULTICENTER, RANDOMIZED, DOUBLE BLIND, PLACEBO CONTROLLE

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The therapeutic options for treatment of AD have thus far focused on modifications of neurotransmitter systems to maximize the remaining activity in neuronal circuits ravaged by the disease. Neurotransmitter-based approaches may provide transient symptomatic benefit for some patients, but do not address the underlying disease process or, ultimately, slow disease progression. The precise cause of the neurodegeneration in AD is currently one of the most intensely investigated issues in neuroscience, and recent advances, in particular, in genetic linkage of familial AD, have strongly suggested that the beta-amyloid protein (A?) may be the causative agent. Multiple arguments support intervention in A? metabolism and/or clearance as a therapeutic approach to the treatment of AD: (1) All known genetically linked forms of AD directly affect either production or deposition of A?; (2) in AD, A? clearance appears to be impaired; and (3) AD is defined as an amyloidosis by the deposition of A?. In other amyloidogenic diseases, it has been shown that limiting production of the amyloid protein leads to its clearance and induces clinical improvement.