22 May Alzheimer’s Disease: Study Finds tau-PET Imaging Increases Diagnostic Accuracy
MedicalResearch.com Interview with:
Dr. Smith
Ruben Smith MD, PhD
Associate professor at Clinical Memory Research
Division of Neurology
Lund University
MedicalResearch.com: What is the background for this study?
Response: Since a few years it has become possible to visualize tau pathology in Alzheimer’s Disease (AD) using positron emission tomography (PET). The tau-PET radiotracer Flortaucipir (Tauvid) was recently approved by the US Food and Drug Administration as an AD diagnostic tool. Since PET imaging is costly and exposes the patient to radioactivity we wanted to study the added clinical value of tau-PET in the diagnostic work-up of patients with cognitive symptoms, before widespread implementation in clinical practice.
MedicalResearch.com: What are the main findings?
Response: The study was designed to prospectively study if tau-PET provided additional information on top of an extensive clinical work-up in participants with cognitive symptoms. The background work-up included all Alzheimer’s Disease biomarkers used in standard clinical practice in southern Sweden, including cerebrospinal fluid (CSF) and blood biomarkers of beta-amyloid and phospho-tau (pTau181). We enrolled 878 patients, referred to secondary Memory Clinics, and found that including tau-PET in the diagnostic work-up resulted in a statistically significant change in diagnosis in 7.5% of the participants and a significant change in medication in 5.5% of the study population.
We also found a significant overall increase in the diagnostic certainty after including tau-PET in the work-up. The results indicate that tau-PET has an added clinical value to increase diagnostic certainty. The results were strongest in beta-amyloid positive patients where AD was a differential diagnosis.
MedicalResearch.com: What should readers take away from your report?
Response: That tau-PET has an added value for diagnostic certainty and to determine whether cognitive symptoms are caused by AD pathology. Just because a patient has started accumulating beta-amyloid and shows evidence of beta-amyloid positivity in blood or cerebrospinal fluid tests it does not necessarily mean that their cognitive symptoms are due to AD. Tau pathology has a stronger association with development of cognitive symptoms and the tau pathology can now reliably be visualized using tau-PET. We found that the tau-PET results led to a significant change in diagnoses and medication of patients and to a significant increase in certainty of underlying etiology when added to an already extensive diagnostic work-up that included CSF AD biomarkers. The effect was largest in beta-amyloid-positive patients. We therefore suggest that clinical use of tau-PET is limited to populations with biomarkers indicating beta-amyloid-positivity.
MedicalResearch.com: What recommendations do you have for future research as a results of this study?
Response: There are many potential studies that could be done as a follow-up to this study. With the emergence of better and more reliable blood biomarkers of AD the use of including blood based biomarkers instead of or in combination with tau-PET should be studied, especially since there could be gains in health economy by using more accessible and cheaper biomarkers. Another important study is to determine how well the visual read paradigms correspond to semi-quantitative measures and if semi-quantitative measures could support or improve the visual reads that are now standard in clinical practice.
Disclosures: The study was supported by the Swedish Research Council, the Knut and Alice Wallenberg foundation, the Marianne and Marcus Wallenberg foundation, the Strategic Research Area MultiPark (Multidisciplinary Research in Parkinson’s disease) at Lund University, the Swedish Alzheimer Foundation, the Swedish Brain Foundation, The Parkinson foundation of Sweden, the Cure Alzheimer’s fund, the Konung Gustaf V:s och Drottning Victorias Frimurarestiftelse, the Skåne University Hospital Foundation, Regionalt Forskningsstöd, the Kockska Foundation, and the Swedish federal government under the ALF agreement. The funding sources had no role in design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication. The precursor of 18F-RO948 was provided by Roche.
Citation:
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