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Over the past decade, there has been an explosion of research describing the relationship between brain β-amyloidosis as measured by PET imaging using 11C–Pittsburgh compound B1 or florbetapir.2 Two articles3,4 in this issue of Neurology® add additional observations. The purpose of this editorial is to describe a conceptual model of Alzheimer disease (AD) pathophysiology that enables the reader to put the current findings into perspective.
ACKNOWLEDGMENT
The author thanks Dr. Clifford Jack for reading an earlier version of this editorial.
Footnotes
Go to Neurology.org for full disclosures. Funding information and disclosures deemed relevant by the author, if any, are provided at the end of the editorial.
- © 2014 American Academy of Neurology
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