PerspectiveNeuroscience

Promiscuous Alzheimer's Amyloid: Yet Another Partner

Science  20 Sep 2013:
Vol. 341, Issue 6152, pp. 1354-1355
DOI: 10.1126/science.1244166

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Summary

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 ortholog, 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.