Alzheimer disease is the leading cause of dementia. The β-amyloid peptide, the core constituent of neuritic plaques found in the brain tissue of patients with the disease, has been identified as a possible causative agent in the pathophysiology of the disease. A variety of therapies are aimed at either reducing the production of this peptide (ie, β- or γ-secretase inhibitors) or improving its clearance from the brain. Recently, immunization with β-amyloid peptide proved remarkably effective in amyloid precursor protein transgenic mouse models of the disease in both preventing the occurrence of plaques and reducing existing pathologic findings in older animals. This immunotherapeutic effect of Aβ appears to be mediated by antibodies against the peptide. These findings have fostered efforts to test this strategy clinically for the possible treatment of Alzheimer disease.
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