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

Read the full 522 word article

How to gain access

Continue reading with a
two-week free trial.