CC BY-NC-ND 4.0 · World J Nucl Med 2021; 20(01): 61-72
DOI: 10.4103/wjnm.WJNM_50_20
Original Article

Analysis of amyloid and tau deposition in Alzheimer's disease using 11C-Pittsburgh compound B and 18F-THK 5351 positron emission tomography imaging

Chotipanich Chanisa
National Cyclotron and PET Centre, Chulabhorn Hospital, Chulabhorn Royal Academy, Bangkok, Thailand
,
Nivorn Monchaya
National Cyclotron and PET Centre, Chulabhorn Hospital, Chulabhorn Royal Academy, Bangkok, Thailand
,
Kunawudhi Anchisa
National Cyclotron and PET Centre, Chulabhorn Hospital, Chulabhorn Royal Academy, Bangkok, Thailand
,
Promteangtrong Chetsadaporn
National Cyclotron and PET Centre, Chulabhorn Hospital, Chulabhorn Royal Academy, Bangkok, Thailand
,
Jantarato Attapon
National Cyclotron and PET Centre, Chulabhorn Hospital, Chulabhorn Royal Academy, Bangkok, Thailand
› Author Affiliations

Abstract

This study aims to determine the deposition of 11C-Pittsburgh compound B (11C-PiB) and 18F-THK 5351 using a normal database of the optimal cut-off-points for standardized uptake value ratios (SUVRs) in Alzheimer's disease (AD) patients. Sixteen AD patients and 24 cognitively normal individuals were enrolled in this study. The optimal cutoff points for the SUVR from the normal database were used for quantitative analysis. P-mod software with the Automated Anatomical Labeling merged atlas was employed to generate automatic volumes of interest to identify different brain regions, and the SUVRs of AD patients were compared with those of the age-matched normal controls. The correlation between PiB and THK5351 deposition at matching brain regions was identified. The mean regional 11C-PiB SUVRs of the AD patients were significantly higher than the healthy controls (P < 0.05). The 11C-PiB SUVR cut-offs were 1.46–1.81, with sensitivity ranging from 81.25% to 93.75% and specificity of 100%. The mean SUVRs of 18F-THK 5351 in various regions were also significantly higher in the AD patients than in the healthy controls (P < 0.05). The inferior temporal gyrus yielded an optimum SUVR cut-off-points of 1.5 with 80% sensitivity and 83.33% specificity. The correlation of PiB and THK5351 SUVR was reported at precuneus, parietal, and occipital brain areas, with spearman's rho of 0.67, 0.66, and 0.72, respectively. Our findings allow determination of the SUVRs of 11C-PiB and 18F-THK-5351 amyloid and tau positron emission tomography tracers for clinical use, according to the normal database of the optimal cut-off-points for SUVRs in AD patients.

Financial support and sponsorship

Chulabhorn Hospital, Chulabhorn Royal Academy.




Publication History

Received: 29 April 2020

Accepted: 16 May 2020

Article published online:
30 March 2022

© 2021. Sociedade Brasileira de Neurocirurgia. This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commecial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/)

Thieme Medical and Scientific Publishers Pvt. Ltd.
A-12, 2nd Floor, Sector 2, Noida-201301 UP, India

 
  • References

  • 1 Betthauser TJ, Lao PJ, Murali D, Barnhart TE, Furumoto S, Okamura N, et al. In vivo comparison of tau radioligands 18 F-THK-5351 and 18 F-THK-5317. J Nucl Med 2017;58:996-1002.
  • 2 Brier MR, Gordon B, Friedrichsen K, McCarthy J, Stern A, Christensen J, et al. Tau and Aβ imaging, CSF measures, and cognition in Alzheimer's disease. Sci Transl Med 2016;8:338ra66.
  • 3 Barc K, Kuźma-Kozakiewicz M. Positron emission tomography neuroimaging in neurodegenerative diseases: Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. Neurol Neurochir Pol 2019;53:99-112.
  • 4 Mayeux R, Stern Y. Epidemiology of Alzheimer disease. Cold Spring Harb Perspect Med 2012;2:a006239. doi: 10.1101/cshperspect.a006239.
  • 5 Okamura N, Harada R, Furumoto S, Arai H, Yanai K, Kudo Y. Tau PET imaging in Alzheimer's disease. Curr Neurol Neurosci Rep 2014;14:500.
  • 6 Mintun MA, Larossa GN, Sheline YI, Dence CS, Lee SY, Mach RH, et al. [11C]PIB in a nondemented population: Potential antecedent marker of Alzheimer disease. Neurology 2006;67:446-52.
  • 7 Rabinovici GD, Furst AJ, O'Neil JP, Racine CA, Mormino EC, Baker SL, et al. 11C-PIB PET imaging in Alzheimer disease and frontotemporal lobar degeneration. Neurology 2007;68:1205-12.
  • 8 Harada R, Okamura N, Furumoto S, Furukawa K, Ishiki A, Tomita N, et al. 18F THK 5351: A novel PET radiotracer for imaging neurofibrillary pathology in Alzheimer disease. J Nucl Med. 2016;57:208-14.
  • 9 Wang YT, Edison P. Tau imaging in neurodegenerative diseases using positron emission tomography. Curr Neurol Neurosci Rep 2019;19:45.
  • 10 Koychev I, Gunn RN, Firouzian A, Lawson J, Zamboni G, Ridha B, et al. PET Tau and amyloid-β burden in mild Alzheimer's Disease: Divergent relationship with age, cognition, and cerebrospinal fluid biomarkers. J Alzheimers Dis 2017;60:283-93.
  • 11 Melis RJF, Haaksma ML, Muniz-Terrera G. Understanding and predicting the longitudinal course of dementia. Curr Opin Psychiatry 2019;32:123-9.
  • 12 McKhann GM, Knopman DS, Chertkow H, Hyman BT, Jack CR Jr., Kawas CH. The diagnosis of dementia due to Alzheimer's disease: Recommendations from the national institute on aging-Alzheimer's association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimers Dement 2011;7:263-9.
  • 13 Rowe CC, Ellis KA, Rimajova M, Bourgeat P, Pike KE, Jones G, et al. Amyloid imaging results from the Australian Imaging, Biomarkers and Lifestyle (AIBL) study of aging. Neurobiol Aging 2010;31:1275-83.
  • 14 Guerreiro R, Bras J. The age factor in Alzheimer's disease. Genome Med 2015;7:106.
  • 15 Hanseeuw BJ, Betensky RA, Jacobs HIL, Schultz AP, Sepulcre J, Becker JA, et al. Association of amyloid and tau with cognition in preclinical Alzheimer disease: A longitudinal study. JAMA Neurol 2019;76:915-24.
  • 16 Koivunen J, Scheinin N, Virta JR, Aalto S, Vahlberg T, Någren K, et al. Amyloid PET imaging in patients with mild cognitive impairment: A 2-year follow-up study. Neurology 2011;76:1085-90.
  • 17 Kemppainen NM, Aalto S, Wilson IA, Någren K, Helin S, Brück A, et al. PET amyloid ligand [11C]PIB uptake is increased in mild cognitive impairment. Neurology 2007;68:1603-6.
  • 18 Chételat G, La Joie R, Villain N, Perrotin A, de La Sayette V, Eustache F, et al. Amyloid imaging in cognitively normal individuals, at-risk populations and preclinical Alzheimer's disease. Neuroimage Clin 2013;2:356-65.
  • 19 Lockhart SN, Baker SL, Okamura N, Furukawa K, Ishiki A, Furumoto S, et al. Dynamic PET measures of tau accumulation in cognitively normal older adults and Alzheimer's disease patients measured using [18F] THK-5351. PLoS One 2016;11:e0158460.
  • 20 Sone D, Imabayashi E, Maikusa N, Okamura N, Furumoto S, Kudo Y, et al. Regional tau deposition and subregion atrophy of medial temporal structures in early Alzheimer's disease: A combined positron emission tomography/magnetic resonance imaging study. Alzheimers Dement (Amst) 2017;9:35-40.
  • 21 Ismail R, Parbo P, Hansen KV, Schaldemose JL, Dalby RB, Tietze A, et al. Abnormal amyloid load in mild cognitive impairment: The effect of reducing the PiB-PET Threshold. J Neuroimaging 2019;29:499-505.
  • 22 Villeneuve S, Rabinovici GD, Cohn-Sheehy BI, Madison C, Ayakta N, Ghosh PM, et al. Existing Pittsburgh Compound-B positron emission tomography thresholds are too high: Statistical and pathological evaluation. Brain 2015;138:2020-33.
  • 23 Jack CR Jr., Wiste HJ, Weigand SD, Therneau TM, Lowe VJ, Knopman DS, et al. Defining imaging biomarker cut points for brain aging and Alzheimer's disease. Alzheimers Dement 2017;13:205-16.
  • 24 Lemoine L, Gillberg PG, Svedberg M, Stepanov V, Jia Z, Huang J, et al. Comparative binding properties of the tau PET tracers THK5117, THK5351, PBB3, and T807 in postmortem Alzheimer brains. Alzheimers Res Ther 2017;9:96.
  • 25 Kikuchi A, Okamura N, Hasegawa T, Harada R, Watanuki S, Funaki Y, et al. In vivo visualization of tau deposits in corticobasal syndrome by 18F-THK5351 PET. Neurology 2016;87:2309-16.
  • 26 Schöll M, Maass A, Mattsson N, Ashton NJ, Blennow K, Zetterberg H, et al. Biomarkers for tau pathology. Mol Cell Neurosci 2019;97:18-33.
  • 27 Thal DR, Rüb U, Orantes M, Braak H. Phases of A beta-deposition in the human brain and its relevance for the development of AD. Neurology 2002;58:1791-800.
  • 28 Ng KP, Pascoal TA, Mathotaarachchi S, Therriault J, Kang MS, Shin M, et al. Monoamine oxidase B inhibitor, selegiline, reduces 18 F-THK5351 uptake in the human brain. Alzheimers Res Ther 2017;9:25.
  • 29 Harada R, Ishiki A, Kai H, Sato N, Furukawa K, Furumoto S, et al. Correlations of 18 F-THK5351 PET with postmortem burden of tau and astrogliosis in Alzheimer Disease. J Nucl Med 2018;59:671-4.