From the Journals

Tau PET tracer distinguishes Alzheimer’s from other disorders


 

FROM JAMA

PET imaging with an investigational tau tracer, 18F-flortaucipir, distinguished Alzheimer’s disease from other neurodegenerative disorders with a high degree of accuracy in a multicenter study.

PET with 18F-flortaucipir also outperformed structural MRI markers for Alzheimer’s disease (AD), and when compared against amyloid-beta (Abeta) biomarkers, showed higher specificity for an AD dementia diagnosis, researchers wrote in a report published online Sept. 18 in JAMA.

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However, the tracer is used only in investigational settings at the moment, wrote Rik Ossenkoppele, PhD, of Lund (Sweden) University and his coinvestigators.

“The accuracy and potential utility of this test in patient care require further research in clinically more representative populations,” they wrote.

The study included 719 participants recruited from memory disorder clinics in Sweden, Korea, and California. That cohort included 179 patients with AD dementia, 254 who had non-AD neurodegenerative diseases, 126 with mild cognitive impairment (MCI), and 160 controls who were cognitively normal. All participants underwent 18F-flortaucipir PET between June 2014 and November 2017.

They found that 18F-flortaucipir showed “high accuracy” for distinguishing AD dementia from non-AD neurodegenerative disorders across all five regions of interest (ROI) evaluated in the study.

For example, 18F-flortaucipir PET had 90.3% accuracy, 89.9% sensitivity, and 90.6% specificity in the temporal meta-ROI, they reported.

By contrast, the accuracy of 18F-flortaucipir was lower for distinguishing MCI caused by AD versus non-AD neurodegenerative conditions. In the temporal meta-ROI, that translated into an 83.4% accuracy, 61.5% sensitivity, and 90.6% specificity, according to the report.

The 18F-flortaucipir tracer outperformed state-of-the-art MRI measures for distinguishing AD dementia from non-AD neurodegenerative disorders, including hippocampal volumes, AD-signature thickness, and whole-brain cortical thickness, Dr. Ossenkoppele and his colleagues found in a secondary analysis.

Likewise, certain analyses showed that specificity for AD dementia versus non-AD neurodegenerative disorders was higher with 18F-flortaucipir than with Abeta status.

While both MRI measures and Abeta status are increasingly used to evaluate cognitive impairment adjunctively in a clinical setting, the utility of 18F-flortaucipir PET as a diagnostic biomarker still must be determined, the investigators wrote in a discussion of their results.

“An intended clinical use of 18F-flortaucipir PET might be to improve the diagnostic work-up as an add-on test to Abeta biomarkers in patients with early-onset dementia and possibly as a triage or even replacement test in patients with late-onset dementia in whom incidental Abeta pathology is common,” they wrote.

The study was sponsored by different sources at each of the clinic sites. Many authors disclosed relationships with companies that are marketing and/or developing PET imaging tracers, including Avid Radiopharmaceuticals/Eli Lilly, GE Healthcare, and Piramal, as well as other pharmaceutical companies.

SOURCE: Ossenkoppele R et al. JAMA. 2018;320(11):1151-62.

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