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Tytuł pozycji:

Visualization of Motor Cortex Involvement by 18F-THK5351 PET Potentially Strengthens Diagnosis of Amyotrophic Lateral Sclerosis.

Tytuł:
Visualization of Motor Cortex Involvement by 18F-THK5351 PET Potentially Strengthens Diagnosis of Amyotrophic Lateral Sclerosis.
Autorzy:
Saitoh Y; From the Department of Neurology, National Center Hospital.
Imabayashi E
Mukai T; From the Department of Neurology, National Center Hospital.
Matsuda H
Takahashi Y; From the Department of Neurology, National Center Hospital.
Źródło:
Clinical nuclear medicine [Clin Nucl Med] 2021 Mar 01; Vol. 46 (3), pp. 243-245.
Typ publikacji:
Case Reports; Journal Article
Język:
English
Imprint Name(s):
Original Publication: Philadelphia, Lippincott.
MeSH Terms:
Aminopyridines*
Positron-Emission Tomography*
Quinolines*
Amyotrophic Lateral Sclerosis/*diagnostic imaging
Motor Cortex/*diagnostic imaging
Aged ; Alzheimer Disease/complications ; Amyotrophic Lateral Sclerosis/complications ; Humans ; Male
References:
Matsuda H, Mizumura S, Nemoto K, et al. Automatic voxel-based morphometry of structural MRI by SPM8 plus diffeomorphic anatomic registration through exponentiated lie algebra improves the diagnosis of probable Alzheimer disease. AJNR Am J Neuroradiol . 2012;33:1109–1114.
Brooks BR, Miller RG, Swash M, et al. El Escorial revisited: revised criteria for the diagnosis of amyotrophic lateral sclerosis. Amyotroph Lateral Scler Other Motor Neuron Disord . 2000;1:293–299.
Van Laere K, Vanhee A, Verschueren J, et al. Value of 18 fluorodeoxyglucose-positron-emission tomography in amyotrophic lateral sclerosis: a prospective study. JAMA Neurol . 2014;71:553–561.
Pagani M, Chio A, Valentini MC, et al. Functional pattern of brain FDG-PET in amyotrophic lateral sclerosis. Neurology . 2014;83:1067–1074.
van Es MA, Hardiman O, Chio A, et al. Amyotrophic lateral sclerosis. Lancet . 2017;390:2084–2098.
Swash M. Why are upper motor neuron signs difficult to elicit in amyotrophic lateral sclerosis? J Neurol Neurosurg Psychitry . 2012;83:659–662.
Ng KP, Pascoal TA, Mathotaarachchi S, et al. Monoamine oxidase B inhibitor, selegiline, reduces 18 F-THK5351 uptake in the human brain. Alzheimers Res Ther . 2017;9:25.
Ishiki A, Harada R, Kai H, et al. Neuroimaging-pathological correlations of [ 18 F]THK5351 PET in progressive supranuclear palsy. Acta Neuropathol Commun . 2018;6:53.
Ng KP, Therriault J, Kang MS, et al. Rasagiline, a monoamine oxidase B inhibitor, reduces in vivo [ 18 F]THK5351 uptake in progressive supranuclear palsy. Neuroimage Clin . 2019;24:102091.
Kushner PD, Stephenson DT, Wright S. Reactive astrogliosis is widespread in the subcortical white matter of amyotrophic lateral sclerosis brain. J Neuropathol Exp Neurol . 1991;50:263–277.
Braak H, Braak E. Neuropathological stageing of Alzheimer-related changes. Acta Neuropathol . 1991;82:239–259.
Alshikho MJ, Zurcher NR, Loggia ML, et al. Glial activation colocalizes with structural abnormalities in amyotrophic lateral sclerosis. Neurology . 2016;87:2554–2561.
Substance Nomenclature:
0 (Aminopyridines)
0 (Quinolines)
0 (THK5351)
Entry Date(s):
Date Created: 20201216 Date Completed: 20210303 Latest Revision: 20230927
Update Code:
20240105
DOI:
10.1097/RLU.0000000000003456
PMID:
33323735
Czasopismo naukowe
Abstract: Amyotrophic lateral sclerosis (ALS) involves both upper motor neurons (UMNs) and lower motor neurons. The detection of UMN involvement, a core component of ALS criteria, is primarily dependent on neurological examination because of a lack of definitive biomarkers. We present the 18F-THK5351 PET images of a 76-year-old man diagnosed with ALS comorbid with Alzheimer disease, demonstrating marked accumulation of 18F-THK5351 in the bilateral precentral gyri. Because 18F-THK5351 binds to monoamine oxidase B highly expressed in astrocytes, where the neurodegenerative process is ongoing, our case highlights that 18F-THK5351 tracer should be a useful marker for detecting UMN neurodegeneration in ALS.
Competing Interests: Conflicts of interest and sources of funding: This study was supported in part by AMED under grant JP20dk0207043 (to Y.S.), by the Intramural Research Grant for Neurological and Psychiatric Disorders of the National Center of Neurology and Psychiatry under grant 30-3 (to Y.S.), and by JSPS KAKENHI under grant 15K09369 (to E.I.) and 15K09981 (to H.M.). The authors declare no conflicts of interest.
(Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.)

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