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Editorial
October 2018

A New Tool for Clinical Neuroscience—Synaptic Imaging

Author Affiliations
  • 1Department of Neurology and Neurological Sciences, Stanford University, Stanford, California
  • 2Helen Wills Neuroscience Institute, University of California, Berkeley, Berkeley
JAMA Neurol. 2018;75(10):1181-1183. doi:10.1001/jamaneurol.2018.1643

The pathogenesis of Alzheimer disease (AD) remains poorly understood and controversial. While a widely adopted framework has proposed that protein aggregates of β-amyloid (Aβ) and tau play key roles in initiating and propagating the disorder,1 many other processes, including cerebrovascular disease and inflammation, have been suggested as etiologically important.2 However, despite these controversies, there has been substantial agreement that AD pathology somehow converges on the synapse. Clinicopathological studies going back almost 3 decades established that synaptic loss is the strongest correlate of cognitive decline measurable in postmortem AD tissue.3,4 Because neural energy is largely expended on signaling,5 and because of associations between glucose utilization and synaptic markers,6 it has been widely believed that positron emission tomography (PET) measurements of glucose hypometabolism with fluorine 18–labeled fluorodeoxyglucose (18F-FDG) reflect synaptic loss in AD. However, until recently, there has been no in vivo method to specifically examine synapses in the human brain.

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