[18F]AV‐1451 tau positron emission tomography in progressive supranuclear palsy
Open accessAbstract
Background: The [18 F]AV‐1451 positron emission tomography ligand allows the in vivo assessment of tau proteins in the brain. It shows strong binding in Alzheimer's dementia, but little is known about how it performs in progressive supranuclear palsy, a primary 4R tauopathy. Objectives: The objectives of this study were to determine whether [18 F]AV‐1451 uptake can be observed in progressive supranuclear palsy and to characterize the regional distribution when compared with controls and Alzheimer's dementia. Methods: [18 F]AV‐1451 positron emission tomography was performed in 10 patients with probable progressive supranuclear palsy. These patients were age‐ and gender‐matched to 50 controls and 10 Alzheimer's dementia patients who had undergone identical [18 F]AV‐1451 imaging. Regional comparisons of [18 F]AV‐1451 uptake were performed across the whole brain using region‐of‐interest and voxel‐level analyses, and correlations between regional [18 F]AV‐1451 and the progressive supranuclear palsy rating scale were assessed. Results: An elevated [18 F]AV‐1451 signal was observed in progressive supranuclear palsy when compared with controls in the pallidum, midbrain, dentate nucleus of the cerebellum, thalamus, caudate nucleus, and frontal regions. Signal in the cerebellar dentate and pallidum were also greater in progressive supranuclear palsy when compared with Alzheimer's dementia. Conversely, the [18 F]AV‐1451 signal across the cortex was higher in Alzheimer's dementia when compared with progressive supranuclear palsy. The [18 F]AV‐1451 signal in a number of regions correlated with the progressive supranuclear palsy rating scale. Conclusions: Progressive supranuclear palsy is associated with an elevated [18 F]AV‐1451 signal in a characteristic and distinct regional pattern that correlates with disease severity and differs from the patterns observed in Alzheimer's dementia. © 2016 International Parkinson and Movement Disorder Society.
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CXCR4 and EGFR demonstrated elevated transcripts within the cerebellum and deep gray nuclei, regions more affected in CBD and PSP than FTD.
“Interestingly, CXCR4 and EGFR demonstrated elevated transcripts within the cerebellum and deep gray nuclei (thalamus and globus pallidus), regions more affected in CBD and PSP than FTD [6, 22, 34].”
From Shared genetic risk between corticobasal degeneration, progressive supranuclear palsy, and frontotemporal dementia (2017) · cites this paper as [34]
The Results (‘PSP compared to controls’; page unavailable) report elevated tau-PET signal in the cerebellar dentate nucleus, thalamus, and pallidum in PSP. The paper does not report CXCR4 or EGFR transcript levels or compare involvement of these regions in CBD, PSP, and FTD. (LLM, conf=0.84)
Experimental — accuracy not yet measuredEarlier PET investigations have detected alterations in PSP with ligands for tau and for microglial activation.
“Previous positron emission tomography (PET) has indicated changes in PSP using ligands targeting tau8–16 and microglial activation17,18.”
From Neuroinflammation and Tau Colocalize in vivo in Progressive Supranuclear Palsy (2020) · cites this paper as [14]
In PSP, higher [18F]AV-1451 binding is found in subcortical rather than cortical regions, consistent with the known distribution of PSP-Richardson's syndrome.
“In PSP, higher [18F]AV-1451 binding has been found in sub-cortical rather than cortical regions (the reverse for AD), consistent with the well-established cortical versus sub-cortical distribution of PSP-Richardson’s syndrome8–10,13,14,16.”
From Neuroinflammation and Tau Colocalize in vivo in Progressive Supranuclear Palsy (2020) · cites this paper as [14]
Only a few previous studies have explored how [11C]PK11195 and [18F]AV-1451 binding relate to disease severity in PSP.
“This finding adds relevant information to the literature as only a few previous studies have explored how [11C]PK11195 and [18F]AV-1451 binding relate to disease severity in PSP8,9,13,14,16,18.”
From Neuroinflammation and Tau Colocalize in vivo in Progressive Supranuclear Palsy (2020) · cites this paper as [14]
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- Authors
- Whitwell, J. L., Lowe, V. J., Tosakulwong, N., Weigand, S. D., Senjem, M. L., Schwarz, C. G., Spychalla, A. J., Petersen, R. C., Jack, C. R., & Josephs, K. A.
- Affiliations
- Mayo Clinic (US)
- Corresponding author
- Whitwell, Jennifer L.
- ORCID
- Venue
- Movement Disorders
- Publisher
- Wiley
- Published
- 2016-10-27
- Volume
- 32
- Issue
- 1
- Pages
- 124-133
- ISSN
- 0885-3185 (ISSN-L)
- 1531-8257
- PMC
- PMC5552410
- OpenAlex
- W2541769071
- Cited by
- 159
- References
- 41
- Citations by year
- 2026: 2 · 2025: 14 · 2024: 14 · 2023: 13 · 2022: 10 · 2021: 20 · 2020: 18 · 2019: 22 · 2018: 21 · 2017: 23 · 2016: 2
- FWCI
- 17.05
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Movement Disorders (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (R01AG034676, U01AG006786, R01AG011378, R01AG037491, R01AG041851, R01AG050603, P50AG016574)
- National Institute on Deafness and Other Communication Disorders (R01DC012519)
- National Institute of Neurological Disorders and Stroke (R01NS089757)
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- progressive supranuclear palsy, 18F-AV-1451, tau PET, tau imaging, Alzheimer's dementia, globus pallidus, dentate nucleus, thalamus, disease severity, neurodegeneration
- MeSH terms
- Aged, Alzheimer Disease, Brain, Carbolines, Female, Humans, Male, Middle Aged, Severity of Illness Index, Supranuclear Palsy, Progressive, tau Proteins, Positron-Emission Tomography
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