A plasticity problem
How β-amyloid could trigger synaptic loss
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