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

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....

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Published inAnnals of neurology Vol. 81; no. 1; pp. 117 - 128
Main Authors 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
Format Journal Article
LanguageEnglish
Published United States Wiley Subscription Services, Inc 01.01.2017
Subjects
Affinity
Age
Aged
Alzheimer's disease
Autopsies
Autopsy
Autoradiography
Axons
Basal ganglia
Binding
Brain
Brain - diagnostic imaging
Brain - metabolism
Brain - pathology
Carbolines - metabolism
Cortex (entorhinal)
Emission analysis
Filaments
Fluorine isotopes
Fluorine Radioisotopes - metabolism
Functional Neuroimaging
Ganglia
Grain
Humans
In vivo methods and tests
Lesions
Ligands
Male
Medical imaging
Mesencephalon
Middle Aged
Mutation
Neurodegenerative diseases
Neurofibrillary tangles
Neuroimaging
Paralysis
Positron emission
Positron emission tomography
Progressive supranuclear palsy
Radioisotopes
Radioligand Assay
Retention
Substantia alba
Substantia nigra
Supranuclear Palsy, Progressive - diagnostic imaging
Supranuclear Palsy, Progressive - pathology
Tau protein
tau Proteins - genetics
tau Proteins - metabolism
Tauopathies - diagnostic imaging
Tauopathies - metabolism
Tauopathies - pathology
Tomography
Tritium - metabolism
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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
AbstractList 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
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
OBJECTIVERecent 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.METHODSWe 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.RESULTSThe 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.INTERPRETATIONAV-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.
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. 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. 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. 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.
Author Lucente, Diane
Bien, Elizabeth A.
Normandin, Marc D.
Gómez‐Isla, Teresa
Siao Tick Chong, Michael
Klunk, William E.
Dickerson, Bradford C.
Meltzer, Avery C.
Mathis, Chester A.
Gomperts, Stephen N.
Johnson, Keith A.
Vanderburg, Charles R.
Frosch, Matthew P.
Domoto‐Reilly, Kimiko
Antón‐Fernández, Alejandro
Marquié, Marta
Oakley, Derek H.
Andrea, Nicolas V.
Costantino, Isabel
Makaretz, Sara
Debnath, Manik
DeVos, Sarah L.
Growdon, John H.
Ikonomovic, Milos D.
Hyman, Bradley T.
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  surname: Marquié
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  fullname: Normandin, Marc D.
  organization: Massachusetts General Hospital
– sequence: 3
  givenname: Avery C.
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  fullname: Meltzer, Avery C.
  organization: Massachusetts General Hospital
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  surname: Siao Tick Chong
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  organization: Massachusetts General Hospital
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  organization: Massachusetts General Hospital
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  organization: University of Pittsburgh School of Medicine
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  organization: University of Pittsburgh School of Medicine
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  organization: University of Pittsburgh School of Medicine
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  fullname: Bien, Elizabeth A.
  organization: Harvard Neurodiscovery Center, Massachusetts General Hospital
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  organization: Harvard Neurodiscovery Center, Massachusetts General Hospital
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  surname: Gómez‐Isla
  fullname: Gómez‐Isla, Teresa
  email: tgomezisla@mgh.harvard.edu
  organization: Massachusetts General Hospital
BackLink https://www.ncbi.nlm.nih.gov/pubmed/27997036$$D View this record in MEDLINE/PubMed
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Snippet Objective Recent studies have shown that positron emission tomography (PET) tracer AV‐1451 exhibits high binding affinity for paired helical filament (PHF)‐tau...
Recent studies have shown that positron emission tomography (PET) tracer AV-1451 exhibits high binding affinity for paired helical filament (PHF)-tau pathology...
Objective Recent studies have shown that positron emission tomography (PET) tracer AV-1451 exhibits high binding affinity for paired helical filament (PHF)-tau...
OBJECTIVERecent studies have shown that positron emission tomography (PET) tracer AV-1451 exhibits high binding affinity for paired helical filament (PHF)-tau...
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StartPage 117
SubjectTerms Affinity
Age
Aged
Alzheimer's disease
Autopsies
Autopsy
Autoradiography
Axons
Basal ganglia
Binding
Brain
Brain - diagnostic imaging
Brain - metabolism
Brain - pathology
Carbolines - metabolism
Cortex (entorhinal)
Emission analysis
Filaments
Fluorine isotopes
Fluorine Radioisotopes - metabolism
Functional Neuroimaging
Ganglia
Grain
Humans
In vivo methods and tests
Lesions
Ligands
Male
Medical imaging
Mesencephalon
Middle Aged
Mutation
Neurodegenerative diseases
Neurofibrillary tangles
Neuroimaging
Paralysis
Positron emission
Positron emission tomography
Progressive supranuclear palsy
Radioisotopes
Radioligand Assay
Retention
Substantia alba
Substantia nigra
Supranuclear Palsy, Progressive - diagnostic imaging
Supranuclear Palsy, Progressive - pathology
Tau protein
tau Proteins - genetics
tau Proteins - metabolism
Tauopathies - diagnostic imaging
Tauopathies - metabolism
Tauopathies - pathology
Tomography
Tritium - metabolism
Title Pathological correlations of [F‐18]‐AV‐1451 imaging in non‐alzheimer tauopathies
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fana.24844
https://www.ncbi.nlm.nih.gov/pubmed/27997036
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Volume 81
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