Over the past several years, experiments with synthetic amyloid-beta peptide (Aβ) and
animal models have strongly suggested that pathogenesis of Alzheimer's disease (AD)
involves soluble assemblies of Aβ peptides (Trends Neurosci. 24 (2001) 219). These
soluble neurotoxins (known as ADDLs and protofibrils) seem likely to account for the
imperfect correlation between insoluble fibrillar amyloid deposits and AD progression.
Recent experiments have detected the presence of ADDLs in AD-afflicted brain tissue and in …