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Editorial
September 2016

Tau and β-Amyloid—The Malignant Duo

Author Affiliations
  • 1School of Public Health, University of California, Berkley
  • 2Helen Wills Neuroscience Institute, University of California, Berkley
JAMA Neurol. 2016;73(9):1049-1050. doi:10.1001/jamaneurol.2016.2481

During the past decade we have experienced an astonishing change in the way we conduct research on Alzheimer disease (AD). Although the importance of the pathologic aggregated proteins—β-amyloid and tau—has long been suspected, understanding their links to symptoms required long-term clinical observation paired with postmortem examination of the brain. As these observations were complemented with imaging of brain structure and function, molecular genetics, and animal models, the amyloid hypothesis of AD has emerged.1 Now that we can measure brain Aβ in living people we have entered a phase of research in which we can test aspects of this hypothesis during life. The recent addition of tau positron emission tomography (PET) imaging has made it possible to examine the interactions between these 2 proteins, which will be crucial to understanding the etiology of AD and its eventual treatment.

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