A 'danse macabre': tau and Fyn in STEP with amyloid beta to facilitate induction of synaptic depression and excitotoxicity. Issue 12 (16th June 2013)

• Record Type: Journal Article
• Authors: Boehm, Jannic
• Is Part Of: European journal of neuroscience. Volume 37:Issue 12(2013:Jun.)
• Page Start: 1925
• Page End: 1930
• Publication Date: 2013-06-16
• Subjects: Nervous system -- Periodicals; 612.8
• DOI: 10.1111/ejn.12251
• Languages: English
• ISSNs: 0953-816X

Abstract

<abstract abstract-type="main" xml:lang="en" id="ejn12251-abs-0001"> <title>Abstract</title> <p>Alzheimer's disease, with its two most prominent pathological factors amyloid beta and tau protein, can be described as a disease of the synapse. It therefore comes as little surprise that NMDA receptor‐related synaptic dysfunction had been thought for several years to underlie the synaptic pathophysiology seen in Alzheimer's disease. In this review I will summarise recent evidence showing that the NMDA receptor links the effects of extracellular amyloid beta with intracellular tau protein. Furthermore, the antagonistic roles of Fyn and STEP in NMDA receptor regulation, synaptic plasticity and induction of synaptic depression will be discussed.</p> </abstract>