Distinct Pools of β-Amyloid in Alzheimer Disease–Affected Brain

Abstract

A critical role of the β-amyloid (Aβ) peptide in the pathogenesis of Alzheimer disease (AD) has been supported by human, animal, and in vitro studies.¹ Most measures of Aβ are markedly elevated in the AD-affected brain, yet the extent of total Aβ accumulation tends to correlate poorly with ADseverity.^2-4 Because there is evidence that specific biochemical forms of Aβ (eg, Aβ₄₂, soluble Aβ, and oligomeric Aβ) selectively lead to neuronal dysfunction and neurodegeneration^5-7 and can be more reliable correlates of clinical status,^8,9 identification and reliable measurement of these toxic Aβ species should enhance their utility as biological markers of disease.