Validating novel tau positron emission tomography tracer [F‐18]‐AV‐1451 (T807) on postmortem brain tissue

Marquié, Marta; Normandin, Marc D.; Vanderburg, Charles R.; Costantino, Isabel M.; Bien, Elizabeth A.; Rycyna, Lisa G.; Klunk, William E.; Mathis, Chester A.; Ikonomovic, Milos D.; Debnath, Manik L.; Vasdev, Neil; Dickerson, Bradford C.; Gomperts, Stephen N.; Growdon, John H.; Johnson, Keith A.; Frosch, Matthew P.; Hyman, Bradley T.; Gómez‐Isla, Teresa

doi:10.1002/ana.24517

Cited by 615Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchMedical Imaging Techniques and Applications

Validating novel tau positron emission tomography tracer [F‐18]‐AV‐1451 (T807) on postmortem brain tissue

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Marquié, Marta, Normandin, Marc D., Vanderburg, Charles R., Costantino, Isabel M., Bien, Elizabeth A., Rycyna, Lisa G., Klunk, William E., Mathis, Chester A. +10 more·2015·Annals of Neurology

DOI 10.1002/ana.24517PMC PMC4900162

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Abstract

Objective: To examine region‐ and substrate‐specific autoradiographic and in vitro binding patterns of positron emission tomography tracer [F‐18]‐AV‐1451 (previously known as T807), tailored to allow in vivo detection of paired helical filament‐tau–containing lesions, and to determine whether there is off‐target binding to other amyloid/non‐amyloid proteins. Methods: We applied [F‐18]‐AV‐1451 phosphor screen autoradiography, [F‐18]‐AV‐1451 nuclear emulsion autoradiography, and [H‐3]‐AV‐1451 in vitro binding assays to the study of postmortem samples from patients with a definite pathological diagnosis of Alzheimer disease, frontotemporal lobar degeneration–tau, frontotemporal lobar degeneration–transactive response DNA binding protein 43 (TDP‐43), progressive supranuclear palsy, corticobasal degeneration, dementia with Lewy bodies, multiple system atrophy, cerebral amyloid angiopathy and elderly controls free of pathology. Results: Our data suggest that [F‐18]‐AV‐1451 strongly binds to tau lesions primarily made of paired helical filaments in Alzheimer brains (eg, intraneuronal and extraneuronal tangles and dystrophic neurites), but does not seem to bind to a significant extent to neuronal and glial inclusions mainly composed of straight tau filaments in non‐Alzheimer tauopathy brains or to lesions containing β‐amyloid, α‐synuclein, or TDP‐43. [F‐18]‐AV‐1451 off‐target binding to neuromelanin‐ and melanin‐containing cells and, to a lesser extent, to brain hemorrhagic lesions was identified. Interpretation: Our data suggest that [F‐18]‐AV‐1451 holds promise as a surrogate marker for the detection of brain tau pathology in the form of tangles and paired helical filament‐tau–containing neurites in Alzheimer brains but also point to its relatively lower affinity for lesions primarily made of straight tau filaments in non‐Alzheimer tauopathy cases and to the existence of some [F‐18]‐AV‐1451 off‐target binding. These findings provide important insights for interpreting in vivo patterns of [F‐18]‐AV‐1451 retention. Ann Neurol 2015 Ann Neurol 2015;78:Ann Neurol 2015;78:679–696

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Previous post-mortem work has demonstrated some binding of 18F-AV-1451 to FTLD pathologies, albeit at a lower magnitude than that seen with Alzheimer's pathology.
“Supporting our use of 18F-AV-1451 as a marker of non-amyloid-β protein aggregation, previous post-mortem work has demonstrated some binding to FTLD pathologies, albeit at a lower magnitude than that seen with Alzheimer’s pathology (Marquié et al., 2015; Lowe et al., 2016; Mcmillan et al., 2016; Sander et al., 2016).”
From Neuroinflammation and protein aggregation co-localize across the frontotemporal dementia spectrum (2020) · cites this paper as Marquié et al., 2015
The Results ([H-3]-AV-1451 binding assays; page unavailable) report lower binding in non-AD tauopathy and TDP-43-containing brain tissue than in AD tissue. But the autoradiography Results found no detectable binding to the FTLD lesions themselves; incidental binding in non-AD cases was associated with age-related PHF tangles. Tissue-level binding therefore does not demonstrate binding to FTLD pathologies. (LLM, conf=0.84)
Experimental — accuracy not yet measured
The molecular target in FTD associated with TDP43 is as yet undetermined, but is unlikely to be TDP43 itself.
“The molecular target in FTD associated with TDP43 is also as yet undetermined, but is unlikely to be TDP43 itself (Marquié et al., 2015; Lowe et al., 2016; Sander et al., 2016).”
From Neuroinflammation and protein aggregation co-localize across the frontotemporal dementia spectrum (2020) · cites this paper as Marquié et al., 2015
The Results (phosphor screen autoradiography; page not provided) report no detectable AV-1451 binding in brain slices containing TDP-43 inclusions, supporting the claim that TDP-43 itself is an unlikely target. The paper does not identify or explicitly discuss an undetermined molecular target for tracer signal in TDP-43-associated FTD; its finding in those slices is largely an absence of binding. (LLM, conf=0.83)
Experimental — accuracy not yet measured
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 [126]
18F-AV-1451 can have other non-tau, non-TDP-43 targets such as neuromelanin and mono-amine oxidase, and such off-target binding is an important caveat in clinical studies using 18F-AV-1451.
“18F-AV-1451 can have other non-tau, non-TDP-43, targets such as neuromelanin (Marquié et al., 2015) and mono-amine oxidase (MAO) (Vermeiren et al., 2018), and such off-target binding is an important caveat in clinical studies using 18F-AV-1451 (Baker et al., 2019).”
From Neuroinflammation and protein aggregation co-localize across the frontotemporal dementia spectrum (2020) · cites this paper as Marquié et al., 2015
The affinity of [18F]AV-1451 for 4-repeat tau in non-AD tauopathies such as PSP is lower than its affinity for 3/4-repeat AD-related tau pathology.
“Nevertheless, we acknowledge that the affinity of [18F]AV-1451 to the 4-repeat tau in non-AD tauopathies as PSP is lower than its affinity to 3/4-repeat AD-related tau pathology29,30.”
From Neuroinflammation and Tau Colocalize in vivo in Progressive Supranuclear Palsy (2020) · cites this paper as [29]

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Frontotemporal lobar degeneration
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Authors: Marquié, M., Normandin, M. D., Vanderburg, C. R., Costantino, I. M., Bien, E. A., Rycyna, L. G., Klunk, W. E., Mathis, C. A., Ikonomovic, M. D., Debnath, M. L., Vasdev, N., Dickerson, B. C., Gomperts, S. N., Growdon, J. H., Johnson, K. A., Frosch, M. P., Hyman, B. T., & Gómez‐Isla, T.
Affiliations: Universitat Autònoma de Barcelona (ES)
Harvard University (US)
Massachusetts General Hospital (US)
University of Pittsburgh (US)
Department of Neurology University of Pittsburgh School of Medicine Pittsburgh PA
Corresponding author: Gómez‐Isla, Teresa
ORCID: Marquié, Marta
Normandin, Marc D.
Vanderburg, Charles R.
Costantino, Isabel M.
Bien, Elizabeth A.
Klunk, William E.
Mathis, Chester A.
Debnath, Manik L.
Vasdev, Neil
Dickerson, Bradford C.
Gomperts, Stephen N.
Johnson, Keith A.
Frosch, Matthew P.
Hyman, Bradley T.
Gómez‐Isla, Teresa
Venue: Annals of Neurology
Publisher: Wiley
Published: 2015-09-25
Volume: 78
Issue: 5
Pages: 787-800
ISSN: 0364-5134 (ISSN-L)
1531-8249
DOI: 10.1002/ana.24517
PMC: PMC4900162
OpenAlex: W2170937822
Cited by: 615
References: 28
Citations by year: 2026: 22 · 2025: 44 · 2024: 20 · 2023: 35 · 2022: 47 · 2021: 65 · 2020: 71 · 2019: 79 · 2018: 72 · 2017: 85 · 2016: 69 · 2015: 5 · 2014: 1
FWCI: 56.75
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: Annals of Neurology (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: NIH (U01NS086659, R01MH100350)
Harvard NeuroDiscovery Center (Boston, MA)
NIH National Institute on Aging (AG005133, AG025204, AG014449, AG005134)
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 › Radiology, Nuclear Medicine and Imaging › Medical Imaging Techniques and Applications
Keywords: tau PET tracers, paired helical filaments, tau pathology, Alzheimer's disease, frontotemporal lobar degeneration, TDP-43, progressive supranuclear palsy, corticobasal degeneration, dementia with Lewy bodies, multiple system atrophy, cerebral amyloid angiopathy, off-target binding, autoradiography, in vitro binding, postmortem brain
MeSH terms: Aged, Aged, 80 and over, Alzheimer Disease, Amyloid, Autoradiography, Brain, Cadaver, Carbolines, Inclusion Bodies, Dementia, Female, Humans, Male, Middle Aged, tau Proteins, Radiopharmaceuticals, Intracranial Hemorrhages, Tauopathies, Positron-Emission Tomography, Frontotemporal Lobar Degeneration, TDP-43 Proteinopathies

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Validating novel tau positron emission tomography tracer [F‐18]‐AV‐1451 (T807) on postmortem brain tissue

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