[ Back to EurekAlert! ] Public release date: 8-May-2013
[ | E-mail Share Share ]

Contact: Jillian Hurst
press_releases@the-jci.org
Journal of Clinical Investigation

Alzheimer's disease is associated with removal of the synaptic protein ADAM10

Alzheimer's disease is characterized by the accumulation of neurotoxic β-amyloid peptide (A-beta). ADAM10, a protein that resides in the neural synapses, has previously been shown to prevent the formation of A-beta. 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

AUTHOR CONTACT:

Monica Di Luca
UniversitÓ degli Studi di Milano, Milano, ITA
Phone: +39-02-50318374; E-mail: monica.diluca@unimi.it

View this article at: http://www.jci.org/articles/view/65401?key=ae8059e94294f112e5b2



[ Back to EurekAlert! ] [ | E-mail Share Share ]

 


AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.