Original Research ARTICLE
Dissociation of Tau Deposits and Brain Atrophy in Early Alzheimer’s Disease: A combined Positron Emission Tomography/Magnetic Resonance Imaging Study
- 1Integrative Brain Imaging Center, National Center of Neurology and Psychiatry (Japan), Japan
- 2Department of Radiology, National Center of Neurology and Psychiatry (Japan), Japan
- 3Department of Neurology, National Center of Neurology and Psychiatry (Japan), Japan
- 4Department of Psychiatry, National Center of Neurology and Psychiatry (Japan), Japan
- 5Division of Pharmacology, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, Japan
- 6Division of Neuro-imaging, Institute of Development, Aging and Cancer, Tohoku University, Japan
- 7Division of Radiopharmaceutical Chemistry, Cyclotron and Radioisotope Center, Tohoku University, Japan
The recent advent of tau-specific positron emission tomography (PET) has enabled in vivo assessment of tau pathology in Alzheimer’s disease (AD). However, because PET scanners have limited spatial resolution, the measured signals of small brain structures or atrophied areas are underestimated by partial volume effects. The aim of this study was to determine whether partial volume correction (PVC) improves the precision of measures of tau deposits in early AD. We investigated tau deposits in 18 patients with amyloid-positive early AD and in 36 amyloid-negative healthy controls using 18F-THK5351 PET. For PVC, we applied the SPM toolbox PETPVE12. The PET images were then spatially normalized and subjected to voxel-based group analysis using SPM12 for comparison between the early AD patients and healthy controls. We also compared these two groups in terms of brain atrophy using voxel-based morphometry of MRI. We found widespread neocortical tracer retention predominantly in the posterior cingulate and precuneus areas, but also in the inferior temporal lobes, inferior parietal lobes, frontal lobes, and occipital lobes in the AD patients compared with the controls. The pattern of tracer retention was similar between before and after PVC, suggesting that PVC had little effect on the precision of tau load measures. Gray matter atrophy was detected in the medial/lateral temporal lobes and basal frontal lobes in the AD patients. Interestingly, only a few associations were found between atrophy and tau deposits, even after PVC. In conclusion, PVC did not significantly affect 18F-THK5351 PET measures of tau deposits. This discrepancy between tau deposits and atrophy suggests that tau load precedes atrophy.
Keywords: Alzheimer’s disease, tau, positron emission tomography, Magnetic Resonance Imaging, partial volume correction, brain atrophy
Received: 11 Sep 2017;
Accepted: 29 Jun 2018.
Edited by:Shin Murakami, Touro University California, United States
Reviewed by:Rik Vandenberghe, KU Leuven, Belgium
Jason Eriksen, University of Houston, United States
Antonio Gambardella, Università degli studi Magna Græcia di Catanzaro, Italy
Copyright: © 2018 Shigemoto, Sone, Imabayashi, Maikusa, Okamura, Furumoto, Kudo, Ogawa, Takano, Yokoi, Sakata, Tsukamoto, Kato, Sato and Matsuda. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: MD. Hiroshi Matsuda, National Center of Neurology and Psychiatry (Japan), Integrative Brain Imaging Center, Tokyo, Japan, firstname.lastname@example.org