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Editorial
September 2002

Explaining the Cause of the Amyloid Burden in Alzheimer Disease

Arch Neurol. 2002;59(9):1367-1368. doi:10.1001/archneur.59.9.1367

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 Aβ plaques and increased Aβ burden over time; Aβ deposition precedes clinical symptoms of AD; Aβ 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 Aβ is neurotoxic in vitro and in vivo; and numerous mutations in β- andγ-secretase genes, and in the APP gene itself, discussed below, are associated with an increased production of Aβ 1–40 and/or Aβ 1–42.120

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