Association Between Alzheimer's Disease And Removal Of The Synaptic Protein ADAM10
In this issue of the Journal of Clinical Investigation, Monica Di Luca and colleagues at the University of Milan in Milan, Italy, report that ADAM10 is removed from synapses through association with the protein AP2. Strikingly, the association between ADAM10 and AP2 was increased in human brain homogenates from Alzheimer's disease (AD) patients compared to healthy controls. Neuronal activity was shown to influence the level and activity of ADAM10 in synapses and its association with AP2.
These studies identify pathological mechanisms associated with AD that control the localization of proteins at the synapse.
TITLE: Endocytosis of synaptic ADAM10 in neuronal plasticity and Alzheimer's disease
View this article at: http://www.jci.org/articles/view/65401?key=ae8059e94294f112e5b2
Adapted by MNT from original media release