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Cited by 628Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchMedical Imaging Techniques and Applications

Tau PET imaging in neurodegenerative tauopathies—still a challenge

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Leuzy, Antoine, Chiotis, Konstantinos, Lemoine, Laetitia, Gillberg, Per-Göran, Almkvist, Ove, Rodriguez-Vieitez, Elena, Nordberg, Agneta·2019·Molecular Psychiatry
DOI 10.1038/s41380-018-0342-8PMC PMC6756230
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Abstract

The accumulation of pathological misfolded tau is a feature common to a collective of neurodegenerative disorders known as tauopathies, of which Alzheimer’s disease (AD) is the most common. Related tauopathies include progressive supranuclear palsy (PSP), corticobasal syndrome (CBS), Down’s syndrome (DS), Parkinson’s disease (PD), and dementia with Lewy bodies (DLB). Investigation of the role of tau pathology in the onset and progression of these disorders is now possible due the recent advent of tau-specific ligands for use with positron emission tomography (PET), including first- (e.g., [ 18 F]THK5317, [ 18 F]THK5351, [ 18 F]AV1451, and [ 11 C]PBB3) and second-generation compounds [namely [ 18 F]MK-6240, [ 18 F]RO-948 (previously referred to as [ 18 F]RO69558948), [ 18 F]PI-2620, [ 18 F]GTP1, [ 18 F]PM-PBB3, and [ 18 F]JNJ64349311 ([ 18 F]JNJ311) and its derivative [ 18 F]JNJ-067)]. In this review we describe and discuss findings from in vitro and in vivo studies using both initial and new tau ligands, including their relation to biomarkers for amyloid-β and neurodegeneration, and cognitive findings. Lastly, methodological considerations for the quantification of in vivo ligand binding are addressed, along with potential future applications of tau PET, including therapeutic trials.

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  • Several tau PET tracers have been developed, including first-generation (18F-AV1451/flortaucipir, 18F-THK family, 11C-PBB3) and newer tracers (18F-MK6240, 18F-R0948, 18F-PI260, 18F-GTP1, 18F-JNJ-64326067).

    “There are several tau PET tracers that have been developed so far with the initial first generation (18F-AV1451/now licensed for clinical use in US as flortaucipir, 18F-THK family and 11C-PBB3) and the newer tracers 18F-MK6240, 18F-R0948, 18F-PI260, 18F-GTP1, and 18F-JNJ-64326067 [178, 179].”

    From The use of neuroimaging techniques in the early and differential diagnosis of dementia (2023) · cites this paper as [179]

    The “First- and second-generation tau tracers” section supports the overall classification and most of the listed tracers, including AV1451 (flortaucipir). It names RO-948, PI-2620 and JNJ64349311, however, rather than the cited sentence’s R0948, PI260 and JNJ-64326067; it also does not establish that flortaucipir is licensed for clinical use in the US. No page number is available in our copy. (LLM, conf=0.90)

    Experimental — accuracy not yet measured

  • Initial tau PET tracers showed good specificity for cortical tau tangles but had evidence of non-specific binding in subcortical structures, suggesting they are not suitable for non-AD tauopathies.

    “The initial tau PET tracers showed good specificity for cortical tau tangles however there has been evidence of non-specific binding in subcortical structures suggesting that tau PET with these tracers is not suitable for non-AD tauopathies [179–183].”

    From The use of neuroimaging techniques in the early and differential diagnosis of dementia (2023) · cites this paper as [179]

    In the sections on in vitro binding and primary tauopathies (page not provided), the paper reports binding to neurofibrillary tangles and off-target binding in the basal ganglia for first-generation tracers. It says this could limit their clinical validity in conditions such as CBS and PSP, but does not conclude that all initial tracers are unsuitable for non-AD tauopathies; it suggests some may be better suited than others for tracking non-AD tau pathology. (LLM, conf=0.87)

    Experimental — accuracy not yet measured

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Authors
Leuzy, A., Chiotis, K., Lemoine, L., Gillberg, P.-G., Almkvist, O., Rodriguez-Vieitez, E., & Nordberg, A.
Affiliations
  • Karolinska Institutet (SE)
  • Karolinska University Hospital (SE)
  • Stockholm University (SE)
Corresponding author
Nordberg, Agneta
ORCID
Venue
Molecular Psychiatry
Publisher
Springer Science and Business Media LLC
Published
2019-01-11
Volume
24
Issue
8
Pages
1112-1134
ISSN
  • 1359-4184 (ISSN-L)
  • 1476-5578
DOI
10.1038/s41380-018-0342-8
PMC
PMC6756230
OpenAlex
W2909883195
Cited by
628
References
33
Citations by year
2026: 45 · 2025: 99 · 2024: 77 · 2023: 66 · 2022: 96 · 2021: 126 · 2020: 92 · 2019: 25
FWCI
9.98
Type
journal article
Language
en
Open access
Licence
Locations
  • Molecular Psychiatry (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
  • Åke Wiberg Stiftelse
  • Demensförbundet (05817)
  • Stiftelsen för Gamla Tjänarinnor (05817, 06086)
  • Stiftelsen för Strategisk Forskning (05817)
  • Yonsei University
  • Lunds Universitet
  • Stockholms Läns Landsting
  • Vetenskapsrådet (02695, 05817, 06086)
  • Université de Genève
  • Yonsei University College of Medicine
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 imaging, tauopathy, Alzheimer's disease, progressive supranuclear palsy, corticobasal syndrome, Down syndrome, Parkinson's disease, dementia with Lewy bodies, [18F]MK-6240, [11C]PBB3, neurodegeneration biomarkers, cognitive impairment
MeSH terms
Alzheimer Disease, Brain, Humans, tau Proteins, Radiopharmaceuticals, Tauopathies, Positron-Emission Tomography

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