A plasticity problem

New research from the University of Bordeaux suggests the synaptic pathology underlying Alzheimer’s disease is driven by aberrant activation of CAMK2 by β-amyloid oligomers. The findings may point to the missing link in how β-amyloid mediates the loss of synaptic receptors and causes defects in synaptic plasticity.

The team’s June paper in Cell Reports showed oligomeric β-amyloid activates calcium calmodulin-dependent protein kinase II (CAMK2) in a way that avoids triggering autophosphorylation and also prevents subsequent normal activation of the protein...