Cortical deposition of amyloid-β (Aβ) peptide is thought to be a crucial early step in the cascade of events leading to Alzheimer’s disease (AD).1 The presence of cortical neuritic plaques, consisting of Aβ fibrils surrounded by degenerating neuronal processes, is a hallmark feature for pathologic diagnosis of AD.2 Aβ plaques have also been identified in individuals meeting clinical criteria for mild cognitive impairment (MCI)3 and have exhibited subtle relationships with cognition among older individuals without dementia or MCI symptoms.4 In addition, pathogenic mutations in genes related to Aβ processing, including the amyloid precursor protein (APP) and presenilin-1 and -2 (PSEN1, PSEN2) genes, have been discovered in patients with the rare, autosomal dominant form of AD.5 As a result, Aβ accumulation is increasingly proposed as a major antecedent ultimately leading to incident AD.6
