Amyloid β and APP as biomarkers for Alzheimer’s disease

Intense research during the past decade has aimed at dissecting the molecular pathogenesis of Alzheimer’s disease (AD). Primarily, the focus has been directed towards brain amyloid pathology and its relation to synaptic and neuronal loss. Clearly, AD is associated with accumulation of amyloid β (Aβ) in the brain. Further, the results of many experimental studies suggest that certain forms of Aβ may act as initiators in the disease process with potent toxic effects at the synaptic level. Molecular aberrations in the AD brain are reflected in the cerebrospinal fluid (CSF). Core CSF biomarkers include secreted Aβ and amyloid precursor protein (APP) isoforms, Aβ oligomers and β-site APP-cleaving enzyme 1 (BACE1). This article reviews recent research advances on CSF and plasma Aβ-related biomarkers for AD and how they may reflect pathogenic changes in AD-affected neuronal networks. We also consider their usefulness in clinical practice and in clinical trials.