Evidence map›Paper›PMID 26996778›Full record

ArticleEuropean journal of nuclear medicine and molecular imaging2016

Imaging in-vivo tau pathology in Alzheimer's disease with THK5317 PET in a multimodal paradigm.

Konstantinos Chiotis, Laure Saint-Aubert, Irina Savitcheva, Vesna Jelic, Pia Andersen, My Jonasson, Jonas Eriksson, Mark Lubberink, Ove Almkvist, Anders Wall and 2 more

Abstract read
In one paragraph

Article in European journal of nuclear medicine and molecular imaging, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 2 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

66 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Review
  6. The Role of Amyloid-β and Tau PET in the New Era of Alzheimer Disease Therapies.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2026
    Review
  7. Article
  8. Article
  9. Review
  10. The tauopathies: Neuroimaging characteristics and emerging experimental therapies.Journal of neuroimaging : official journal of the American Society of Neuroimaging · 2022
    Review
  11. International consensus on the use of tau PET imaging agentEuropean journal of nuclear medicine and molecular imaging · 2022
    Article
  12. Frontiers in aging neuroscience · 2022
    Article
  13. Article
  14. Imaging pathological tau in atypical parkinsonisms: A review.Clinical parkinsonism & related disorders · 2022
    Review
  15. Review
  16. [Molecular psychiatry · 2021
    Article
  17. Review
  18. Review
  19. Article
  20. Review

6 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Konstantinos ChiotisDepartment NVS, Center for Alzheimer Research, Division of Translational Alzheimer Neurobiology, Karolinska Institutet, Novum 5th floor, 141 57, Huddinge, Sweden.
Laure Saint-AubertDepartment NVS, Center for Alzheimer Research, Division of Translational Alzheimer Neurobiology, Karolinska Institutet, Novum 5th floor, 141 57, Huddinge, Sweden.
Irina SavitchevaDepartment of Radiology, Karolinska University Hospital Huddinge, Stockholm, Sweden.
Vesna JelicDepartment of Geriatric Medicine, Karolinska University Hospital Huddinge, Stockholm, Sweden.
Pia AndersenDepartment of Geriatric Medicine, Karolinska University Hospital Huddinge, Stockholm, Sweden.
My JonassonRadiology, Department of Surgical Sciences, Uppsala University, Uppsala, Sweden.
Jonas ErikssonPET Centre, Uppsala University Hospital, Uppsala, Sweden.
Mark LubberinkRadiology, Department of Surgical Sciences, Uppsala University, Uppsala, Sweden.
Ove AlmkvistDepartment NVS, Center for Alzheimer Research, Division of Translational Alzheimer Neurobiology, Karolinska Institutet, Novum 5th floor, 141 57, Huddinge, Sweden.
Anders WallRadiology, Department of Surgical Sciences, Uppsala University, Uppsala, Sweden.
Gunnar AntoniPET Centre, Uppsala University Hospital, Uppsala, Sweden.
Agneta NordbergDepartment NVS, Center for Alzheimer Research, Division of Translational Alzheimer Neurobiology, Karolinska Institutet, Novum 5th floor, 141 57, Huddinge, Sweden. Agneta.K.Nordberg@ki.se.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThe aim of this study was to explore the cerebral distribution of the tau-specific PET tracer [(18)F]THK5317 (also known as (S)-[(18)F]THK5117) retention in different stages of Alzheimer's disease; and study any associations with markers of hypometabolism and amyloid-beta deposition.

methodsThirty-three individuals were enrolled, including nine patients with Alzheimer's disease dementia, thirteen with mild cognitive impairment (MCI), two with non-Alzheimer's disease dementia, and nine healthy controls (five young and four elderly). In a multi-tracer PET design [(18)F]THK5317, [(11)C] Pittsburgh compound B ([(11)C]PIB), and [(18)F]FDG were used to assess tau pathology, amyloid-beta deposition and cerebral glucose metabolism, respectively. The MCI patients were further divided into MCI [(11)C]PIB-positive (n = 11) and MCI [(11)C]PIB-negative (n = 2) groups.

resultsTest-retest variability for [(18)F]THK5317-PET was very low (1.17-3.81 %), as shown by retesting five patients. The patients with prodromal (MCI [(11)C]PIB-positive) and dementia-stage Alzheimer's disease had significantly higher [(18)F]THK5317 retention than healthy controls (p = 0.002 and p = 0.001, respectively) in areas exceeding limbic regions, and their discrimination from this control group (using the area under the curve) was >98 %. Focal negative correlations between [(18)F]THK5317 retention and [(18)F]FDG uptake were observed mainly in the frontal cortex, and focal positive correlations were found between [(18)F]THK5317 and [(11)C]PIB retentions isocortically. One patient with corticobasal degeneration syndrome and one with progressive supranuclear palsy showed no [(11)C]PIB but high [(18)F]THK5317 retentions with a different regional distribution from that in Alzheimer's disease patients.

conclusionsThe tau-specific PET tracer [(18)F]THK5317 images in vivo the expected regional distribution of tau pathology. This distribution contrasts with the different patterns of hypometabolism and amyloid-beta deposition.

Indexed as

Aniline CompoundsMultimodal ImagingPositron-Emission TomographyQuinolinesAdultAgedAlzheimer DiseaseAmyloid beta-PeptidesCase-Control StudiesFemaleHumansMaleMiddle AgedRadioactive TracersYoung Adult6-((3-fluoro-2-hydroxy)propoxy)-2-(4-methylaminophenyl)quinolineAmyloid beta-PeptidesAniline CompoundsQuinolinesRadioactive TracersAlzheimer’s diseaseAmyloid PETFDGNeurofibrillary tanglesNon-ADOther dementiaPIBPositron emission tomographyTauTHK5317

Identifiers

PMID26996778
PMCPMC4932128

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.