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Arch Neurol. 2002;59:1367-1368.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

THE DEPOSITION of amyloid in the progression of Alzheimer disease (AD) has emerged as one of the central constructs in the pathogenesis of AD. The primary role of altered amyloidogenesis in the causation of AD has been supported convincingly by data from several investigators. Support for the amyloid hypothesis as a primary cause for altered cognition and progressive dementia in AD includes the following statements: brains with AD contain increased numbers of A plaques and increased A burden over time; A deposition precedes clinical symptoms of AD; A is increased in the plasma of persons older than 65 years who later develop AD compared with age-matched controls; patients with Down syndrome develop AD because of an extra copy of the amyloid precursor protein (APP) gene on chromosome 21; fibrillar A is neurotoxic in vitro and in vivo; and numerous mutations in - and-secretase genes, and in the . . . [Full Text of this Article]

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