Using Tau Imaging as Diagnostic Marker for Alzheimer Disease

EMBARGOED FOR RELEASE: 11 A.M (ET), MONDAY, JULY 25, 2016

Media Advisory: To contact corresponding study author Beau M. Ances, M.D., Ph.D., call Judy Martin at 314-286-0105 or email martinju@wustl.edu. To contact corresponding editorial author William Jagust, M.D., call Robert Sanders at 510-642-3734 or email rlsanders@berkeley.edu.

To place an electronic embedded link in your story: Links will be live at the embargo time: http://archneur.jamanetwork.com/article.aspx?doi=10.1001/jamaneurol.2016.2078; http://archneur.jamanetwork.com/article.aspx?doi=10.1001/jamaneurol.2016.2481

 

JAMA Neurology 

The accumulation of β-Amyloid (Αβ) and tau proteins in the brain is hallmark pathology for Alzheimer disease. Recently developed positron emission tomography (PET) tracers, including [18F]-AV-1451, bind to tau in neurofibrillary tangles in the brain. So, could tau imaging become a diagnostic marker for Alzheimer disease and provide insights into the pathophysiology of the neurodegenerative disorder that destroys brain cells?

In a new article published online by JAMA Neurology, Beau M. Ances, M.D., Ph.D., of Washington University, St. Louis, and coauthors examined the usefulness of [18F]-AV-1451 PET imaging to stage AD and assess associations among Αβ, tau and volume loss in the brain.

The imaging study included 59 participants, the majority of whom were older men, who were cognitively normal or who had Alzheimer dementia.

The authors report that PET imaging using [18F]-AV-1451 distinguished participants with Alzheimer from those who were cognitively normal. Also, an elevated [18F]-AV-1451 binding was associated with volume loss in parts of the brain, according to the study.

“Overall, our work suggests that [18F]-AV-1451 is a valuable tool in tracking the continuum of the neurodegenerative process that ranges from the preclinical to clinical phase of AD,” the article concludes.

To read the full study and a related editorial, “Tau and β-Amyloid – The Malignant Duo,” by William Jagust, M.D., of the University of California, Berkley, please visit the For The Media website.

(JAMA Neurol. Published online July 25, 2016. doi:10.1001/jamaneurol.2016.2078. Available pre-embargo to the media at http://media.jamanetwork.com.)

Editor’s Note: The article contains conflict of interest and funding/support disclosures. Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.

 

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