18 F-AV-1451 tau PET imaging correlates strongly with tau neuropathology in MAPT mutation carriers
Open accessAbstract
Tau positron emission tomography ligands provide the novel possibility to image tau pathology in vivo However, little is known about how in vivo brain uptake of tau positron emission tomography ligands relates to tau aggregates observed post-mortem. We performed tau positron emission tomography imaging with (18)F-AV-1451 in three patients harbouring a p.R406W mutation in the MAPT gene, encoding tau. This mutation results in 3- and 4-repeat tau aggregates similar to those in Alzheimer's disease, and many of the mutation carriers initially suffer from memory impairment and temporal lobe atrophy. Two patients with short disease duration and isolated memory impairment exhibited (18)F-AV-1451 uptake mainly in the hippocampus and adjacent temporal lobe regions, correlating with glucose hypometabolism in corresponding regions. One patient died after 26 years of disease duration with dementia and behavioural deficits. Pre-mortem, there was (18)F-AV-1451 uptake in the temporal and frontal lobes, as well as in the basal ganglia, which strongly correlated with the regional extent and amount of tau pathology in post-mortem brain sections. Amyloid-β ((18)F-flutemetamol) positron emission tomography scans were negative in all cases, as were stainings of brain sections for amyloid. This provides strong evidence that (18)F-AV-1451 positron emission tomography can be used to accurately quantify in vivo the regional distribution of hyperphosphorylated tau protein.
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In vivo studies show 18F-AV-1451 binding in areas typically affected in FTD and affected at post-mortem, and elevated binding in affected brain regions of patients with svPPA and bvFTD due to C9orf72 expansions.
“This is corroborated by in vivo studies of patients with a straight filament 4-repeat tauopathy and clinical FTD resulting from MAPT mutations, showing binding in areas typically affected in FTD and affected at post-mortem (Bevan-Jones et al., 2016; Smith et al., 2016), and by the elevated binding in the affected brain regions of patients with svPPA (Bevan-Jones et al., 2018a, Makaretz et al., 201”
From Neuroinflammation and protein aggregation co-localize across the frontotemporal dementia spectrum (2020) · cites this paper as Smith et al., 2016
The Results and Discussion report 18F-AV-1451 binding in temporal and frontal regions of MAPT R406W carriers and a strong correlation with post-mortem tau pathology in one patient. However, the Discussion describes their aggregates as containing both 3R and 4R tau, including paired helical filaments—not a straight-filament 4-repeat tauopathy. The svPPA and C9orf72 portion of the citing sentence is attached to other citations, not Smith et al. (LLM, conf=0.88)
Experimental — accuracy not yet measuredStudies 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 [ <sup>18</sup> F]flortaucipir and Postmortem Assessment of Alzheimer Disease Neuropathologic Changes (2020) · cites this paper as [30]
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 [ <sup>18</sup> F]flortaucipir and Postmortem Assessment of Alzheimer Disease Neuropathologic Changes (2020) · cites this paper as [30]
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- Authors
- Smith, R., Puschmann, A., Schöll, M., Ohlsson, T., van Swieten, J., Honer, M., Englund, E., & Hansson, O.
- Affiliations
- Lund University (SE)
- Skåne University Hospital (SE)
- F. Hoffmann-La Roche AG (CH)
- Corresponding author
- Smith, Ruben
- Hansson, Oskar
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2016-06-29
- Volume
- 139
- Issue
- 9
- Pages
- 2372-2379
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- PMC
- PMC4995360
- OpenAlex
- W2474047710
- Cited by
- 168
- References
- 5
- Citations by year
- 2026: 1 · 2025: 10 · 2024: 4 · 2023: 11 · 2022: 18 · 2021: 23 · 2020: 22 · 2019: 21 · 2018: 22 · 2017: 27 · 2016: 9
- FWCI
- 21.20
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc
- Locations
- Brain (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (acceptedVersion, other-oa)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion, other-oa)
- RePub (Erasmus University Rotterdam) (submittedVersion, other-oa)
- UCL Discovery (University College London) (submittedVersion)
- Lund University Publications (Lund University) (submittedVersion)
- HighWire Press Open Archive (submittedVersion)
- RePub (Erasmus University Rotterdam) (submittedVersion)
- Funders
- Australian Government
- Vetenskapsrådet
- Avid Radiopharmaceuticals (AV-1451)
- 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, hyperphosphorylated tau, tau aggregates, tauopathy, glucose hypometabolism, behavioral variant frontotemporal dementia
- MeSH terms
- Aged, Atrophy, Carbolines, Dementia, Female, Heterozygote, Hippocampus, Humans, Male, Memory Disorders, Middle Aged, Mutation, Temporal Lobe, tau Proteins, Positron-Emission Tomography
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