Promiscuous Alzheimer's Amyloid: Yet Another Partner

摘要

Although genetic evidence puts the amyloid peptide ( β-amyloid or Aβ) center stage in Alzheimer's disease (AD), it remains far from clear how this 4-kD protein fragment compromises neuronal function (1). On page 1399 of this issue, Kim et al. identify two new receptors for aggregated Aβ: the mouse paired immunoglobulin-like receptor B (PirB) and its human ortho-log, leukocyte immunoglobulin-like receptor LilrB2 (2). The binding interaction triggers a signaling cascade that compromises the actin cytoskeleton of neurons and ultimately causes synaptic loss in a mouse model of AD.