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Neurobiol Aging. 2017 Nov;59:210-219. doi: 10.1016/j.neurobiolaging.2017.08.008. Epub 2017 Aug 12.

Tau positron emission tomography using [18F]THK5351 and cerebral glucose hypometabolism in Alzheimer's disease.

Author information

1
Department of Psychiatry, Gachon University Gil Medical Center, Incheon, Republic of Korea.
2
Department of Neuroscience, College of Medicine, Gachon University, Incheon, Republic of Korea.
3
Neuroscience Research Institute, Gachon University, Incheon, Republic of Korea.
4
Department of Neurology, Gachon University Gil Medical Center, Incheon, Republic of Korea.
5
Department of Nuclear Medicine, Seoul National University Hospital, Seoul National University College of Medicine, Republic of Korea.
6
Tohoku Medical and Pharmaceutical University, Sendai, Japan.
7
Cyclotron and Radioisotope Center, Tohoku University, Sendai, Japan.
8
Tohoku Medical and Pharmaceutical University, Sendai, Japan; Cyclotron and Radioisotope Center, Tohoku University, Sendai, Japan.
9
Department of Molecular Imaging and Therapy, Centre for PET, Austin Health, Melbourne, Victoria, Australia; The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Melbourne, Victoria, Australia.
10
Department of Biomedical Engineering, Korea University, Seoul, Republic of Korea; Department of Brain and Cognitive Engineering, Korea University, Seoul, Republic of Korea.
11
Department of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea; Neuroscience Center, Samsung Medical Center, Seoul, Republic of Korea.
12
Department of Occupational and Environmental Medicine, Gachon University Gil Medical Center, Incheon, Republic of Korea.
13
Department of Neurology, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Republic of Korea. Electronic address: kmin.lee33@gmail.com.
14
Department of Neurology, Gachon University Gil Medical Center, Incheon, Republic of Korea; Department of Health Science and Technology, GAIHST, Gachon University, Incheon, Republic of Korea. Electronic address: ynoh@gachon.ac.kr.

Abstract

This study aims to evaluate the clinical validity of [18F]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 [18F]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, [18F]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. [18F]THK5351 retention significantly correlated with neuropsychological test results. Negative correlations between [18F]THK5351 and [18F] fluorodeoxyglucose were observed in AD dementia and aMCI groups. Mirror images of [18F]THK5351 retention and glucose hypometabolism in [18F] fluorodeoxyglucose were noticeable in the focal variants of AD. [18F]THK5351 PET reflects disease severity and symptoms in AD. Our results suggest [18F]THK5351 is reflective of tau-related AD pathology.

KEYWORDS:

Alzheimer's disease; Neurofibrillary tangles; Positron emission tomography; THK; Tau

[Indexed for MEDLINE]

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