New PET Tracer Discriminates Alzheimer's From Other Neurodegenerative Disorders

September 19, 2018

By Will Boggs MD 

NEW YORK—18F-flortaucipir, a PET tracer that allows in vivo quantification of paired helical filament tau, accurately differentiates Alzheimer's disease (AD) from other neurodegenerative disorders, researchers report.

"Tau PET was clearly superior to established MRI measures when distinguishing patients with Alzheimer's disease from other neurodegenerative disorders, and showed higher specificity compared to amyloid-beta PET," Dr. Rik Ossenkoppele from Lund University in Sweden and VU University Medical Center in Amsterdam, the Netherlands, and Dr. Oskar Hansson from Lund University told Reuters Health in a joint email.

Initial human 18F-flortaucipir PET studies showed good discrimination between patients with AD and controls, but the accuracy for distinguishing AD from non-AD neurodegenerative disorders remained unclear.

Dr. Ossenkoppele, Dr. Hansson and their colleagues used data from 719 participants, including 179 with AD dementia, 254 with non-AD neurodegenerative disorders, 126 with mild cognitive impairment (MCI), and 160 cognitively normal controls to examine the diagnostic performance of 18F-flortaucipir PET (tau PET).

For all brain regions of interest, mean 18F-flortaucipir standardized uptake values ratios (SUVRs) were significantly higher in the AD dementia group compared with all other groups, the researchers report in the September 18 issue of JAMA.

SUVRs were higher in MCI due to AD compared with non-AD neurodegenerative disorder and control groups and did not differ significantly between non-AD neurodegenerative disorders and controls.

18F-flortaucipir showed high accuracy for discriminating AD dementia from the combined group of non-AD neurodegenerative disorders. In the temporal region of interest, for example, 18F-flortaucipir discriminated AD from non-AD neurodegenerative disorders with 90.3% accuracy, 89.9% sensitivity and 90.6% specificity.

Specificity was somewhat lower for differentiating AD dementia from dementia with Lewy bodies and semantic variant primary progressive aphasia.

Discriminative accuracy was also lower for MCI due to AD versus non-AD neurodegenerative conditions than for AD dementia versus non-AD neurodegenerative conditions.

18F-flortaucipir's discriminative accuracy was higher than that of MRI markers and CSF amyloid-beta measures for distinguishing AD dementia from non-AD neurodegenerative disorders.

"We think that tau PET imaging will improve the diagnostic work-up at many memory clinics in the near future and might replace some less accurate assessments that are routinely used in current clinical practice," Dr. Ossenkoppele and Dr. Hansson said.

"If a patient presents with memory impairment and mild to moderate dementia and the tau PET scan is abnormal, it is very probable that Alzheimer's disease causes the syndrome. In contrast, if the tau PET scan appears to be normal, the syndrome is most likely due to another type of dementia," they said.

"Tau PET tracers are currently solely used in investigational settings," they added. "The present study in conjunction with post-mortem studies verifying in vivo tau PET signal may facilitate the approval of tau PET tracers for clinical purposes in the next few years."

Dr. Takeshi Iwatsubo from Graduate School of Medicine at the University of Tokyo, who recently described Japanese and North American efforts to harmonize Alzheimer's disease neuroimaging studies, told Reuters Health by email, "Tau pathology in AD dementia and prodromal AD (MCI due to AD) can be sensitively detected by flortaucipir PET, and incorporation of flortaucipir in AD diagnosis together with amyloid PET, CSF analysis, MRI, in addition to clinical evaluation, will improve the precision in differential diagnosis of dementing disorders." Dr. Iwatsubo was not part of the new study.

SOURCE: https://bit.ly/2PO93ma

JAMA 2018.

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