Pathological correlations of [F‐18]‐AV‐1451 imaging in non‐alzheimer tauopathies

Marquié, Marta; Normandin, Marc D.; Meltzer, Avery C.; Siao Tick Chong, Michael; Andrea, Nicolas V.; Antón‐Fernández, Alejandro; Klunk, William E.; Mathis, Chester A.; Ikonomovic, Milos D.; Debnath, Manik; Bien, Elizabeth A.; Vanderburg, Charles R.; Costantino, Isabel; Makaretz, Sara; DeVos, Sarah L.; Oakley, Derek H.; Gomperts, Stephen N.; Growdon, John H.; Domoto‐Reilly, Kimiko; Lucente, Diane; Dickerson, Bradford C.; Frosch, Matthew P.; Hyman, Bradley T.; Johnson, Keith A.; Gómez‐Isla, Teresa

doi:10.1002/ana.24844

Cited by 190Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchParkinson's Disease Mechanisms and Treatments

Pathological correlations of [F‐18]‐AV‐1451 imaging in non‐alzheimer tauopathies

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Marquié, Marta, Normandin, Marc D., Meltzer, Avery C., Siao Tick Chong, Michael, Andrea, Nicolas V., Antón‐Fernández, Alejandro, Klunk, William E., Mathis, Chester A. +17 more·2017·Annals of Neurology

DOI 10.1002/ana.24844PMC PMC5319193

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Abstract

Objective: Recent studies have shown that positron emission tomography (PET) tracer AV‐1451 exhibits high binding affinity for paired helical filament (PHF)‐tau pathology in Alzheimer's brains. However, the ability of this ligand to bind to tau lesions in other tauopathies remains controversial. Our goal was to examine the correlation of in vivo and postmortem AV‐1451 binding patterns in three autopsy‐confirmed non‐Alzheimer tauopathy cases. Methods: We quantified in vivo retention of [F‐18]‐AV‐1451 and performed autoradiography, [H‐3]‐AV‐1451 binding assays, and quantitative tau measurements in postmortem brain samples from two progressive supranuclear palsy (PSP) cases and a MAPT P301L mutation carrier. They all underwent [F‐18]‐AV‐1451 PET imaging before death. Results: The three subjects exhibited [F‐18]‐AV‐1451 in vivo retention predominantly in basal ganglia and midbrain. Neuropathological examination confirmed the PSP diagnosis in the first two subjects; the MAPT P301L mutation carrier had an atypical tauopathy characterized by grain‐like tau‐containing neurites in gray and white matter with heaviest burden in basal ganglia. In all three cases, autoradiography failed to show detectable [F‐18]‐AV‐1451 binding in multiple brain regions examined, with the exception of entorhinal cortex (reflecting incidental age‐related neurofibrillary tangles) and neuromelanin‐containing neurons in the substantia nigra (off‐target binding). The lack of a consistent significant correlation between in vivo [F‐18]‐AV‐1541 retention and postmortem in vitro binding and tau measures in these cases suggests that this ligand has low affinity for tau lesions primarily made of straight tau filaments. Interpretation: AV‐1451 may have limited utility for in vivo selective and reliable detection of tau aggregates in these non‐Alzheimer tauopathies. ANN NEUROL 2017;81:117–128

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Flortaucipir binds weakly or not at all to sole 4R or sole 3R tau deposits in primary tauopathies.
“Flortaucipir binds weakly or not at all to sole 4R or sole 3R tau deposits in primary tauopathies [126–128].”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [128]
Studies comparing antemortem tau positron emission tomography imaging with autopsy have begun assessing the ability of flortaucipir to detect underlying neurofibrillary tangles in Alzheimer disease and non-Alzheimer disease dementias.
“Studies comparing antemortem tau PET imaging with autopsy have begun assessing the ability of flortaucipir to detect underlying NFTs in AD and non-AD dementias.25,26,27,28,29,30,31,32,33”
From Positron Emission Tomography Imaging With [ 18 F]flortaucipir and Postmortem Assessment of Alzheimer Disease Neuropathologic Changes (2020) · cites this paper as [27]
Flortaucipir appears to bind poorly to non-AD tau pathologies such as those seen in frontotemporal dementias, progressive supranuclear palsy, corticobasal degeneration, and chronic traumatic encephalopathy.
“[18F]flortaucipir appears to bind poorly to non-AD tau pathologies such as those seen in frontotemporal dementias, progressive supranuclear palsy, corticobasal degeneration, and chronic traumatic encephalopathy.27,30,32,50,56,57”
From Positron Emission Tomography Imaging With [ 18 F]flortaucipir and Postmortem Assessment of Alzheimer Disease Neuropathologic Changes (2020) · cites this paper as [27]

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Authors: Marquié, M., Normandin, M. D., Meltzer, A. C., Siao Tick Chong, M., Andrea, N. V., Antón‐Fernández, A., Klunk, W. E., Mathis, C. A., Ikonomovic, M. D., Debnath, M., Bien, E. A., Vanderburg, C. R., Costantino, I., Makaretz, S., DeVos, S. L., Oakley, D. H., Gomperts, S. N., Growdon, J. H., Domoto‐Reilly, K., Lucente, D., Dickerson, B. C., Frosch, M. P., Hyman, B. T., Johnson, K. A., & Gómez‐Isla, T.
Affiliations: Massachusetts General Hospital (US)
MassGeneral Institute for NeuroDegenerative Disease Charlestown MA
University of Pittsburgh (US)
Department of Neurology University of Pittsburgh School of Medicine Pittsburgh PA
Harvard NeuroDiscovery Center (US)
Corresponding author: Gómez‐Isla, Teresa
ORCID: Marquié, Marta
Normandin, Marc D.
Antón‐Fernández, Alejandro
Klunk, William E.
Mathis, Chester A.
Debnath, Manik
Bien, Elizabeth A.
Vanderburg, Charles R.
Costantino, Isabel
DeVos, Sarah L.
Oakley, Derek H.
Gomperts, Stephen N.
Domoto‐Reilly, Kimiko
Lucente, Diane
Dickerson, Bradford C.
Frosch, Matthew P.
Hyman, Bradley T.
Johnson, Keith A.
Gómez‐Isla, Teresa
Venue: Annals of Neurology
Publisher: Wiley
Published: 2017-01
Volume: 81
Issue: 1
Pages: 117-128
ISSN: 0364-5134 (ISSN-L)
1531-8249
DOI: 10.1002/ana.24844
PMC: PMC5319193
OpenAlex: W2566270954
Cited by: 190
References: 9
Citations by year: 2026: 3 · 2025: 7 · 2024: 8 · 2023: 17 · 2022: 18 · 2021: 28 · 2020: 26 · 2019: 24 · 2018: 34 · 2017: 25
FWCI: 22.28
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor, 23 d)
Locations: Annals of Neurology (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: Harvard NeuroDiscovery Center
Topics: Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
Keywords: tau PET imaging, progressive supranuclear palsy, off-target binding, basal ganglia, entorhinal cortex
MeSH terms: Aged, Autoradiography, Brain, Carbolines, Fluorine Radioisotopes, Humans, Male, Middle Aged, Mutation, Radioligand Assay, Supranuclear Palsy, Progressive, Tritium, tau Proteins, Tauopathies, Positron-Emission Tomography, Functional Neuroimaging

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Pathological correlations of [F‐18]‐AV‐1451 imaging in non‐alzheimer tauopathies

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