The characteristic pathological signature of AD noted by Alzheimer is the presence of deposits of Aft peptide in extracellular plaques accompanied by tau deposits in intracellular tangles. The weight of the genetic evidence from familial forms of AD supports the Aft peptide as a prime mover in the etiology of the disease (Hardy and Selkoe, 2002). While it is clear that mutations in /APP can cause AD in the genetic cases, sporadic AD must involve other factors. If it is true that multimeric A/ is either an initiating factor and/or a chronic stressor, strategies to alleviate these effects should alter the course of the disease.
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