In vivo tau PET imaging in dementia: Pathophysiology, radiotracer quantification, and a systematic review of clinical findings
Open accessAbstract
In addition to the deposition of β-amyloid plaques, neurofibrillary tangles composed of aggregated hyperphosphorylated tau are one of the pathological hallmarks of Alzheimer's disease and other neurodegenerative disorders. Until now, our understanding about the natural history and topography of tau deposition has only been based on post-mortem and cerebrospinal fluid studies, and evidence continues to implicate tau as a central driver of downstream neurodegenerative processes and cognitive decline. Recently, it has become possible to assess the regional distribution and severity of tau burden in vivo with the development of novel radiotracers for positron emission tomography (PET) imaging. In this article, we provide a comprehensive discussion of tau pathophysiology, its quantification with novel PET radiotracers, as well as a systematic review of tau PET imaging in normal aging and various dementia conditions: mild cognitive impairment, Alzheimer's disease, frontotemporal dementia, progressive supranuclear palsy, and Lewy body dementia. We discuss the main findings in relation to group differences, clinical-cognitive correlations of tau PET, and multi-modal relationships among tau PET and other pathological markers. Collectively, the small but growing literature of tau PET has yielded consistent anatomical patterns of tau accumulation that recapitulate post-mortem distribution of neurofibrillary tangles which correlate with cognitive functions and other markers of pathology. In general, AD is characterised by increased tracer retention in the inferior temporal lobe, extending into the frontal and parietal regions in more severe cases. It is also noted that the spatial topography of tau accumulation is markedly distinct to that of amyloid burden in aging and AD. Tau PET imaging has also revealed characteristic spatial patterns among various non-AD tauopathies, supporting its potential role for differential diagnosis. Finally, we propose novel directions for future tau research, including (a) longitudinal imaging in preclinical dementia, (b) multi-modal mapping of tau pathology onto other pathological processes such as neuroinflammation, and (c) the need for more validation studies against post-mortem samples of the same subjects.
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Overall, tau PET deposition mirrors progression of AD pathology and correlates with disease severity.
“Overall, tau PET deposition mirrors the progression of AD pathology, correlates with disease severity and in that respect it is hypothesised that will become one of the most important tools for the differential diagnosis between AD and non-AD dementias [191, 199, 200].”
From The use of neuroimaging techniques in the early and differential diagnosis of dementia (2023) · cites this paper as [200]
The ligand [18F]AV-1451 binds aggregated tau in Alzheimer's disease and, less avidly, in non-Alzheimer tauopathies.
“The latter binds to aggregated tau in Alzheimer’s disease (AD) and, with lower affinity, to non-AD tauopathies21.”
From Neuroinflammation and Tau Colocalize in vivo in Progressive Supranuclear Palsy (2020) · cites this paper as [21]
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Reference Tissue–Based Kinetic Evaluation of 18F-AV-1451 for Tau Imaging
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Temporal T807 binding correlates with CSF tau and phospho-tau in normal elderly
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Pharmacokinetic Evaluation of the Tau PET Radiotracer 18F-T807 (18F-AV-1451) in Human Subjects
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Self-citationAdvances in the development of tau PET radiotracers and their clinical applications
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Self-citationVisualization of regional tau deposits using 3H-THK5117 in Alzheimer brain tissue
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Self-citationModeling Strategies for Quantification of In Vivo 18F-AV-1451 Binding in Patients with Tau Pathology
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Self-citationElevated in vivo [18F]‐AV‐1451 uptake in a patient with progressive supranuclear palsy
Hammes, J., Bischof, G. N., Giehl, K., Faber, J., Drzezga, A., Klockgether, T., & van Eimeren, T. (2017) · Movement Disorders · doi:10.1002/mds.26727 · Cited by 49 · see citing works
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[<sup>18</sup>F]AV‐1451 PET in behavioral variant frontotemporal dementia due to MAPT mutation
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Flagged first, then by citations
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- Authors
- Hall, B., Mak, E., Cervenka, S., Aigbirhio, F. I., Rowe, J. B., & O’Brien, J. T.
- Affiliations
- University of Cambridge (GB)
- MRC Cognition and Brain Sciences Unit (GB)
- Venue
- Ageing Research Reviews
- Publisher
- Elsevier BV
- Published
- 2017-07
- Volume
- 36
- Pages
- 50-63
- ISSN
- 1568-1637 (ISSN-L)
- OpenAlex
- W2601835166
- Cited by
- 132
- References
- 117
- Citations by year
- 2026: 3 · 2025: 9 · 2024: 14 · 2023: 11 · 2022: 9 · 2021: 15 · 2020: 20 · 2019: 21 · 2018: 20 · 2017: 10
- FWCI
- 2.94
- Type
- journal article
- Language
- en
- Open access
- Licence
- cc-by-nc-nd
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- Locations
- Ageing Research Reviews (publishedVersion)
- PubMed (publishedVersion)
- Apollo (University of Cambridge) (submittedVersion, cc-by-nc-nd)
- Apollo
- Funders
- Wellcome Trust (103838)
- 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
- tau PET imaging, neurofibrillary tangles, hyperphosphorylated tau, Alzheimer's disease, dementia, mild cognitive impairment, frontotemporal dementia, progressive supranuclear palsy, dementia with Lewy bodies, tauopathy, normal aging, inferior temporal lobe, amyloid, differential diagnosis, cognitive decline, neuroinflammation, preclinical dementia
- MeSH terms
- Alzheimer Disease, Animals, Dementia, Fluorine Radioisotopes, Humans, Temporal Lobe, Biomarkers, Neurofibrillary Tangles, tau Proteins, Neurodegenerative Diseases, Tauopathies, Positron-Emission Tomography, Plaque, Amyloid, Cognitive Dysfunction
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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