Discriminative Accuracy of [ 18 F]flortaucipir Positron Emission Tomography for Alzheimer Disease vs Other Neurodegenerative Disorders
Open accessAbstract
Importance: The positron emission tomography (PET) tracer [18F]flortaucipir allows in vivo quantification of paired helical filament tau, a core neuropathological feature of Alzheimer disease (AD), but its diagnostic utility is unclear. Objective: To examine the discriminative accuracy of [18F]flortaucipir for AD vs non-AD neurodegenerative disorders. Design, Setting, and Participants: In this cross-sectional study, 719 participants were recruited from 3 dementia centers in South Korea, Sweden, and the United States between June 2014 and November 2017 (160 cognitively normal controls, 126 patients with mild cognitive impairment [MCI], of whom 65.9% were amyloid-β [Aβ] positive [ie, MCI due to AD], 179 patients with AD dementia, and 254 patients with various non-AD neurodegenerative disorders). Exposures: The index test was the [18F]flortaucipir PET standardized uptake value ratio (SUVR) in 5 predefined regions of interest (ROIs). Cut points for tau positivity were determined using the mean +2 SDs observed in controls and Youden Index for the contrast AD dementia vs controls. Main Outcomes and Measures: The reference standard was the clinical diagnosis determined at the specialized memory centers. In the primary analysis, the discriminative accuracy (ie, sensitivity and specificity) of [18F]flortaucipir was examined for AD dementia vs all non-AD neurodegenerative disorders. In secondary analyses, the area under the curve (AUC) of [18F]flortaucipir SUVR was compared with 3 established magnetic resonance imaging measures (hippocampal volumes and AD signature and whole-brain cortical thickness), and sensitivity and specificity of [18F]flortaucipir in MCI due to AD vs non-AD neurodegenerative disorders were determined. Results: Among 719 participants, the overall mean (SD) age was 68.8 (9.2) years and 48.4% were male. The proportions of patients who were amyloid-β positive were 26.3%, 65.9%, 100%, and 23.8% among cognitively normal controls, patients with MCI, patients with AD dementia, and patients with non-AD neurodegenerative disorders, respectively. [18F]flortaucipir uptake in the medial-basal and lateral temporal cortex showed 89.9% (95% CI, 84.6%-93.9%) sensitivity and 90.6% (95% CI, 86.3%-93.9%) specificity using the threshold based on controls (SUVR, 1.34), and 96.8% (95% CI, 92.0%-99.1%) sensitivity and 87.9% (95% CI, 81.9%-92.4%) specificity using the Youden Index-derived cutoff (SUVR, 1.27) for distinguishing AD dementia from all non-AD neurodegenerative disorders. The AUCs for all 5 [18F]flortaucipir ROIs were higher (AUC range, 0.92-0.95) compared with the 3 volumetric MRI measures (AUC range, 0.63-0.75; all ROIs P < .001). Diagnostic performance of the 5 [18F]flortaucipir ROIs were lower in MCI due to AD (AUC range, 0.75-0.84). Conclusions and Relevance: Among patients with established diagnoses at a memory disorder clinic, [18F]flortaucipir PET was able to discriminate AD from other neurodegenerative diseases. The accuracy and potential utility of this test in patient care require further research in clinically more representative populations.
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Structural MRI represents a relatively lower-cost alternative to spatially measure in vivo neurodegeneration, but it is substantially less specific to AD pathology compared to PET.
“Structural magnetic resonance imaging (MRI) represents a relatively lower‐cost alternative to spatially measure in vivo neurodegeneration, but it is substantially less specific to AD pathology compared to PET. 5 , 6 , 7 , 8”
From Machine learning prediction of tau‐PET in Alzheimer's disease using plasma, MRI, and clinical data (2025) · cites this paper as [5]
The introduction identifies structural MRI as a biomarker of neurodegeneration that lacks specificity for AD. The “Flortaucipir PET vs MRI Markers” section reports substantially better discrimination of AD dementia from other neurodegenerative disorders with flortaucipir PET than with MRI atrophy measures. The copy mentions higher costs associated with PET, but does not establish a direct MRI-versus-PET cost comparison; its comparison is also specific to flortaucipir PET, rather than PET generally. (LLM, conf=0.86)
Experimental — accuracy not yet measured18F-flortaucipir PET showed slightly lower accuracy (AUC 0.75-0.84) when comparing positive amyloid PET MCI to other non-AD neurodegenerative disorders.
“It did show however slightly lower accuracy (AUC 0.75–0.84) when comparing positive amyloid PET MCI to other non-AD neurodegenerative disorders [192].”
From The use of neuroimaging techniques in the early and differential diagnosis of dementia (2023) · cites this paper as [192]
The MCI Due to AD vs Non-AD Neurodegenerative Disorders section reports lower flortaucipir PET accuracy than in AD dementia, with AUCs of 0.75–0.84 across five regions. However, the Participants section says amyloid positivity was determined by PET or cerebrospinal fluid testing; the reported AUC range is not specific to amyloid-PET-positive MCI. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIn a multicentre cross-sectional study of 719 participants, 18F-flortaucipir PET had 89.9% sensitivity and 90.6% specificity in discriminating AD from non-AD neurodegenerative disorders.
“In a multicentre cross-sectional study that included 719 participants (150 controls, 126 MCI, 170 AD and 254 other neurodegenerative disorder), 18F-flortaucipir PET had 89.9% sensitivity and 90.6% specificity in discriminating AD from non-AD neurodegenerative disorders and higher AUC (0.92–0.95) compared to volumetric MRI measures (AUC 0.63–0.75) [192].”
From The use of neuroimaging techniques in the early and differential diagnosis of dementia (2023) · cites this paper as [192]
Table 2 reports 89.9% sensitivity and 90.6% specificity for distinguishing AD dementia from non-AD neurodegenerative disorders; the Results also report the stated PET and MRI AUC ranges. However, the citing sentence misstates the group counts: the study had 160 controls and 179 patients with AD dementia, not 150 and 170 (Participants; Abstract, page unavailable). (LLM, conf=0.92)
Experimental — accuracy not yet measured18F-flortaucipir PET had higher AUC (0.92-0.95) compared to volumetric MRI measures (AUC 0.63-0.75) in that study.
“In a multicentre cross-sectional study that included 719 participants (150 controls, 126 MCI, 170 AD and 254 other neurodegenerative disorder), 18F-flortaucipir PET had 89.9% sensitivity and 90.6% specificity in discriminating AD from non-AD neurodegenerative disorders and higher AUC (0.92–0.95) compared to volumetric MRI measures (AUC 0.63–0.75) [192].”
From The use of neuroimaging techniques in the early and differential diagnosis of dementia (2023) · cites this paper as [192]
Aschenbrenner et al. retrospectively studied 152 participants; only tau PET signal significantly predicted cognitive decline, while high amyloid levels were also associated with tau-related cognitive decline.
“Aschenbrenner et al. 131 performed a retrospective study of 152 participants who had received at least 1 flortaucipir tau PET scan and 1 florbetapir amyloid PET scan within a year, and ≥2 clinical and cognitive assessments.All participants entering the study had equal to or less than 0.5 on the CDR scale; that is, they were cognitively normal or with very mild AD.The statistical analysis demonstr”
From The amyloid hypothesis in Alzheimer disease: new insights from new therapeutics (2022) · cites this paper as [131]
Tau PET may continue to increase throughout the disease course, which gives it a very high diagnostic accuracy during the later stage of the disease.
“Tau PET may continue to increase throughout the disease course, which gives it a very high diagnostic accuracy during the later stage of the disease (36).”
From Aβ deposition is associated with increases in soluble and phosphorylated tau that precede a positive tau PET in Alzheimer's disease (2020) · cites this paper as [36]
Approximately 20% (19%-23%) of participants with positive amyloid PET scans have no or low levels of flortaucipir binding by quantitative or visual interpretation.
“Similarly, approximately 20% (19%-23%) of participants with positive amyloid PET scans have no or low levels of [18F]flortaucipir binding by quantitative or visual interpretation.21,23,50,51,52”
From Positron Emission Tomography Imaging With [ <sup>18</sup> F]flortaucipir and Postmortem Assessment of Alzheimer Disease Neuropathologic Changes (2020) · cites this paper as [50]
A multinational flortaucipir F18 imaging study that evaluated 719 participants with clinical diagnoses of AD dementia, non-AD neurodegenerative disorders, and mild cognitive impairment as well as controls with normal cognition demonstrated a high level of discriminative accuracy of flortaucipir for AD compared with other neurocognitive disorders.
“A multinational flortaucipir F18 imaging study that evaluated 719 participants with clinical diagnoses of AD dementia, non-AD neurodegenerative disorders, and mild cognitive impairment as well as controls with normal cognition demonstrated a high level of discriminative accuracy of [18F]flortaucipir for AD compared with other neurocognitive disorders.50”
From Positron Emission Tomography Imaging With [ <sup>18</sup> F]flortaucipir and Postmortem Assessment of Alzheimer Disease Neuropathologic Changes (2020) · cites this paper as [50]
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Self-citationBiomarkers for neurodegenerative diseases
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Self-citationAdvancing Research and Treatment for Frontotemporal Lobar Degeneration (ARTFL) investigators, Thijssen, E. H., La Joie, R., Wolf, A., Strom, A., Wang, P., Iaccarino, L., Bourakova, V., Cobigo, Y., Heuer, H., et al. (2020) · Nature Medicine · doi:10.1038/s41591-020-0762-2 · Cited by 761 · see citing works
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Plasma GFAP is an early marker of amyloid-β but not tau pathology in Alzheimer's disease
Pereira, J. B., Janelidze, S., Smith, R., Mattsson-Carlgren, N., Palmqvist, S., Teunissen, C. E., Zetterberg, H., Stomrud, E., Ashton, N. J., Blennow, K., et al. (2021) · Brain · doi:10.1093/brain/awab223 · Cited by 598 · see citing works
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Self-citationAmyloid-β-independent regulators of tau pathology in Alzheimer disease
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Self-citationBlood biomarkers for Alzheimer’s disease in clinical practice and trials
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Time course of phosphorylated-tau181 in blood across the Alzheimer’s disease spectrum
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Self-citationThe use of neuroimaging techniques in the early and differential diagnosis of dementia
Chouliaras, L., & O’Brien, J. T. (2023) · Molecular Psychiatry · doi:10.1038/s41380-023-02215-8 · Cited by 186 · see citing works
“…(150 controls, 126 MCI, 170 AD and 254 other neurodegenerative disorder), 18 F-fl ortaucipir PET had 89.9% sensitivity and 90.6% speci fi city in discriminating AD from non-AD neurodegenerative disorders and higher AUC (0.92 – 0.95) compared to volumetric MRI measures (AUC 0.63 – 0.75) [ 192].”
ResultInfluentialOssenkoppele, R., Lyoo, C. H., Jester-Broms, J., Sudre, C. H., Cho, H., Ryu, Y. H., Choi, J. Y., Smith, R., Strandberg, O., Palmqvist, S., et al. (2020) · JAMA Neurology · doi:10.1001/jamaneurol.2019.5154 · Cited by 161 · see citing works
Alzheimer’s disease profiled by fluid and imaging markers: tau PET best predicts cognitive decline
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Correlation of In Vivo [<sup>18</sup>F]Flortaucipir With Postmortem Alzheimer Disease Tau Pathology
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Head-to-head comparison of tau positron emission tomography tracers [18F]flortaucipir and [18F]RO948
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Self-citationPlasma Phospho‐Tau Identifies Alzheimer's Co‐Pathology in Patients with Lewy Body Disease
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Self-citationNuclear medicine and molecular imaging advances in the 21st century
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Self-citationAssociation of plasma P-tau181 with memory decline in non-demented adults
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Self-citationMachine learning prediction of tau‐PET in Alzheimer's disease using plasma, MRI, and clinical data
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Self-citation
- Authors
- Ossenkoppele, R., Rabinovici, G. D., Smith, R., Cho, H., Schöll, M., Strandberg, O., Palmqvist, S., Mattsson, N., Janelidze, S., Santillo, A., Ohlsson, T., Jögi, J., Tsai, R., La Joie, R., Kramer, J., Boxer, A. L., Gorno-Tempini, M. L., Miller, B. L., Choi, J. Y., Ryu, Y. H., Lyoo, C. H., & Hansson, O.
- Affiliations
- Lund University (SE)
- University of California, San Francisco (US)
- Yonsei University (KR)
- Skåne University Hospital (SE)
- Memory and Aging Center, Department of Neurology, University of California San Francisco
- Corresponding author
- Ossenkoppele, Rik
- Hansson, Oskar
- ORCID
- Venue
- JAMA
- Publisher
- American Medical Association (AMA)
- Published
- 2018-09-18
- Volume
- 320
- Issue
- 11
- Pages
- 1151
- ISSN
- 0002-9955 (ISSN-L)
- 0098-7484
- PMC
- PMC6233630
- OpenAlex
- W2892120842
- Cited by
- 472
- References
- 51
- Citations by year
- 2026: 51 · 2025: 74 · 2024: 58 · 2023: 60 · 2022: 56 · 2021: 73 · 2020: 57 · 2019: 37 · 2018: 6
- FWCI
- 33.49
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- JAMA (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion)
- Pure Amsterdam UMC (acceptedVersion, other-oa)
- YUHSpace (Yonsei University Medical Library) (submittedVersion, cc-by-nc-nd)
- Lund University Publications (Lund University) (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Funders
- Alzheimer's Association (P50 AG023501, 443577, AARF-16-443577, 16-443577)
- Larry L. Hillblom Foundation
- Amgen
- Bristol-Myers Squibb
- Parkinson Research Foundation
- Eli Lilly and Company
- Pfizer
- American Brain Foundation (R01-AG045611)
- Biogen
- Celgene
- Quest Diagnostics
- TauRx Pharmaceuticals
- National Institute for Health and Care Research
- National Research Foundation
- Lunds Universitet
- Ministry of Science, ICT and Future Planning (2017R1A2B2006694, 2015R1C1A2A01054507)
- National Research Foundation of Korea (2017R1A2B2006694, 2015R1C1A2A01054507)
- Knut och Alice Wallenbergs Stiftelse
- Vetenskapsrådet
- Skånes universitetssjukhus
- Marcus och Amalia Wallenbergs minnesfond
- National Institutes of Health
- Genentech
- University of California, San Francisco
- Parkinsonfonden
- Avid Radiopharmaceuticals
- NIHR Cambridge Biomedical Research Centre
- National Institute on Aging (R01AG045611, R01AG038791, U01AG052943, P01AG019724, P30AG062422, R01AG032289, P50AG023501)
- National Institute on Deafness and Other Communication Disorders (K24DC015544)
- National Institute of Neurological Disorders and Stroke (R01NS100440, R56NS050915, U54NS092089, R01NS050915)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Medical Imaging Techniques and Applications
- Keywords
- 18F-flortaucipir, Alzheimer's disease, tau PET imaging, discriminative accuracy, mild cognitive impairment, amyloid-beta, hippocampal volume, cortical thickness, dementia diagnosis, standardized uptake value ratio, sensitivity and specificity, differential diagnosis of dementia, neurodegeneration biomarkers
- MeSH terms
- Adult, Aged, Aged, 80 and over, Alzheimer Disease, Carbolines, Cerebral Cortex, Cross-Sectional Studies, Diagnosis, Differential, Female, Humans, Male, Middle Aged, Sensitivity and Specificity, Amyloid beta-Peptides, Radiopharmaceuticals, Area Under Curve, Neurodegenerative Diseases, Fluorodeoxyglucose F18, Positron-Emission Tomography, Cognitive Dysfunction
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