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Tau positron emission tomography using [18F]THK5351 and cerebral glucose hypometabolism in Alzheimer's disease
Kang JM, Lee SY, Seo S, Jeong HJ, Woo SH, Lee H, Lee YB, Yeon BK et al.. Neurobiology of aging, 2017-08-12
Topic: Brain proteins, microglia and lab models
This study aims to evaluate the clinical validity of [ 18 F]THK5351 positron emission tomography (PET) for the assessment of disease progression and symptoms in Alzheimer's disease (AD). Fifty-one patients with AD dementia, 30 patients with amnestic mild cognitive impairment (aMCI), and 43 controls with normal cognition (NC) were included. All subjects underwent [ 18 F]THK5351 PET, 3.0-T magnetic resonance imaging, and detailed neuropsychological tests. Regions of interest and voxel-based statistical analyses were performed. In patients with AD dementia, [ 18 F]THK5351 retention was greater in most association cortices as well as the limbic area compared to NC or aMCI participants. Patients with aMCI also showed higher THK5351 retention in those areas compared to NC. [ 18 F]THK5351 retention significantly correlated with neuropsychological test results. Negative correlations between [ 18 F]THK5351 and [ 18 F] fluorodeoxyglucose were observed in AD dementia and aMCI groups. Mirror images of [ 18 F]THK5351 retention and glucose hypometabolism in [ 18 F] fluorodeoxyglucose were noticeable in the focal variants of AD. [ 18 F]THK5351 PET reflects disease severity and symptoms in AD. Our results suggest [ 18 F]THK5351 is reflective of tau-related AD pathology.
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APA 7th
Kang, J. M., Lee, S. Y., Seo, S., Jeong, H. J., Woo, S. H., Lee, H., et al. (2017). Tau positron emission tomography using [18F]THK5351 and cerebral glucose hypometabolism in Alzheimer's disease. Neurobiology of aging. https://doi.org/10.1016/j.neurobiolaging.2017.08.008
Vancouver
Kang JM, Lee SY, Seo S, Jeong HJ, Woo SH, Lee H, et al. Tau positron emission tomography using [18F]THK5351 and cerebral glucose hypometabolism in Alzheimer's disease. Neurobiology of aging. 2017. doi:10.1016/j.neurobiolaging.2017.08.008. PMID: 28890300.
BibTeX
@article{kang2017-28890300,
author = {Kang, J. M. and Lee, S. Y. and Seo, S. and Jeong, H. J. and Woo, S. H. and Lee, H. and Lee, Y. B. and Yeon, B. K. and others},
title = {{Tau positron emission tomography using [18F]THK5351 and cerebral glucose hypometabolism in Alzheimer's disease}},
journal = {Neurobiology of aging},
year = {2017},
doi = {10.1016/j.neurobiolaging.2017.08.008},
pmid = {28890300},
url = {https://doi.org/10.1016/j.neurobiolaging.2017.08.008}
}
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Key findings
- In patients with AD dementia, [ 18 F]THK5351 retention was greater in most association cortices as well as the limbic area compared to NC or aMCI participants.
- Patients with aMCI also showed higher THK5351 retention in those areas compared to NC. [ 18 F]THK5351 retention significantly correlated with neuropsychological test results.
- Our results suggest [ 18 F]THK5351 is reflective of tau-related AD pathology.
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Study details
- Participants30
- Evidence strengthLow
How this study scored 45/100
Published in a peer-reviewed journal. Scored zero for study design, effect reported and randomised / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multi-centre collaboration, so those were left out: it earned 26 of the 58 points we could judge it on, which is 45 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Neurobiology of aging) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 2 / 5 | 2017 — within 10 year(s) of the newest study here |
| Sample size | 1 / 4 | 30 participants |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 3 / 3 | Studied in people (participant count stated) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 28890300) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 26 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 26 of the 58 points we could judge it on is 45 out of 100. |
| Total | 45 / 100 | — |
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