title: The amyloid precursor protein intracellular domain-fe65 multiprotein complexes: a challenge to the amyloid hypothesis for Alzheimer's disease?
abstract: Since its proposal in 1994, the amyloid cascade hypothesis has prevailed as the mainstream research subject on the molecular mechanisms leading to the Alzheimer's disease (AD). Most of the field had been historically based on the role of the different forms of aggregation of β-amyloid peptide (Aβ). However, a soluble intracellular fragment termed amyloid precursor protein (APP) intracellular domain (AICD) is produced in conjunction with Aβ fragments. This peptide had been shown to be highly toxic in both culture neurons and transgenic mice models. With the advent of this new toxic fragment, the centerpiece for the ethiology of the disease may be changed. This paper discusses the potential role of multiprotein complexes between the AICD and its adapter protein Fe65 and how this could be a potentially important new agent in the neurodegeneration observed in the AD.
authors.affiliation: Laboratory of Cell and Neuronal Dynamics, Department of Biology and Institute for Cell Dynamics and Biotechnology (ICDB), Faculty of Sciences, Universidad de Chile, Santiago 7800024, Chile.
authors.forename: Daniel A
authors.initials: DA
authors.lastname: Bórquez
authors.forename: Christian
authors.initials: C
authors.lastname: González-Billault