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

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